Subjects -> BIOLOGY (Total: 3174 journals)
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CYTOLOGY AND HISTOLOGY (32 journals)

Showing 1 - 29 of 29 Journals sorted alphabetically
Acta Histochemica     Hybrid Journal   (Followers: 3)
Annals of Cytology and Pathology     Open Access   (Followers: 1)
Applied Immunohistochemistry & Molecular Morphology     Hybrid Journal   (Followers: 16)
Cell Discovery     Open Access   (Followers: 2)
Comparative Cytogenetics     Open Access   (Followers: 1)
Current Protocols in Cytometry     Hybrid Journal  
Cytogenetic and Genome Research     Full-text available via subscription   (Followers: 2)
Cytokine     Hybrid Journal   (Followers: 6)
Cytokine & Growth Factor Reviews     Hybrid Journal   (Followers: 3)
Cytokine : X     Open Access  
Cytology and Genetics     Hybrid Journal   (Followers: 4)
Cytometry Part A     Hybrid Journal   (Followers: 3)
Cytometry Part B: Clinical Cytometry     Hybrid Journal   (Followers: 4)
Cytopathology     Hybrid Journal   (Followers: 11)
Cytoskeleton     Hybrid Journal   (Followers: 1)
Cytotechnology     Hybrid Journal   (Followers: 10)
Diagnostic Cytopathology     Hybrid Journal   (Followers: 10)
Egyptian Journal of Genetics And Cytology     Open Access  
European Journal of Histochemistry     Open Access   (Followers: 4)
Folia Cryptogamica Estonica     Open Access  
Histochemistry and Cell Biology     Hybrid Journal   (Followers: 6)
Journal of Cytology & Histology     Open Access   (Followers: 5)
Journal of Histochemistry and Cytochemistry     Hybrid Journal   (Followers: 7)
Journal of Histotechnology     Hybrid Journal   (Followers: 2)
Journal of Molecular Histology     Hybrid Journal   (Followers: 5)
Journal of the American Society of Cytopathology     Hybrid Journal   (Followers: 5)
Journal of the History of Biology     Hybrid Journal   (Followers: 5)
Single Cell Biology     Open Access  
Vegetation History and Archaeobotany     Hybrid Journal   (Followers: 4)
Similar Journals
Journal Cover
Cytotechnology
Journal Prestige (SJR): 0.519
Citation Impact (citeScore): 1
Number of Followers: 10  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0920-9069 - ISSN (Online) 1573-0778
Published by Springer-Verlag Homepage  [2469 journals]
  • N1-methylpseudouridine-incorporated mRNA enhances exogenous protein
           expression and suppresses immunogenicity in primary human fibroblast-like
           synoviocytes

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      Abstract: Abstract Studies conducted using murine arthritis models have indicated that the use of in vitro-transcribed messenger RNA (IVT mRNA) is an effective therapeutic approach for joint diseases. However, the use of IVT mRNA in human synovial cells has not been widely studied. Recently, the outbreak of the novel coronavirus disease has accelerated the development of innovative mRNA vaccines, such as those containing a modified nucleic acid, N1-methylpseudouridine-5′-triphosphate (m1ψ). IVT mRNA is an attractive tool for biological experiments and drug discovery. To verify the protein expression from IVT mRNA in vitro, primary cultured fibroblast-like synoviocytes (FLS) and MH7A human synovial fibroblast cells were transfected with enhanced green fluorescent protein (EGFP) mRNA with or without m1ψ incorporation. EGFP was detected using western blotting and fluorescence microscopy. A multiplex assay was performed to comprehensively understand IVT mRNA-induced immunogenicity. Gene expression levels were measured using reverse transcription polymerase chain reaction. In both MH7A cells and FLS, cells transfected with EGFP mRNA containing m1ψ generated higher levels of EGFP than those transfected with unmodified EGFP or control mRNAs. The multiplex assay of the FLS culture supernatant and reverse transcription polymerase chain reaction for FLS revealed that both concentration and expression of IL-6, TNF-α, and CXCL10 were upregulated by unmodified EGFP mRNA, whereas they were suppressed by EGFP mRNA with m1ψ. Overall, m1ψ incorporation enhanced protein expression and decreased the expression of cytokines. These findings may contribute to arthritis research.
      PubDate: 2022-06-30
       
  • Soft substrate maintains stemness and pluripotent stem cell-like phenotype
           of human embryonic stem cells under defined culture conditions

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      Abstract: Abstract Human embryonic stem cells (hESCs) are derived from the inner cell mass (ICM) of the pre-implantation blastocyst. Prior to embryo implantation, the ICM cells are surrounded by trophoblasts which have mechanical stiffness ranging from Pascal (Pa) to kilopascal (kPa). However, under in vitro conditions these cells are cultured on stiff tissue culture treated plastic plates (TCP) which have stiffness of approximately 1 gigapascal (GPa). This obvious dichotomy motivated us to investigate the fate of hESCs cultured on softer substrate, and to probe if the hESCs undergo differentiation or they retain pluripotency on soft substrates. We investigated the expression of pluripotency markers, and lineage-specific markers; we particularly looked at the expression of transcriptional coactivator YAP (Yes-associated protein), an important mediator of extracellular matrix (ECM) mechanical cues and a known downstream transducer of Hippo pathway. Downregulation of YAP has been correlated to the loss of multipotency of human mesenchymal stem cells (hMSCs) and pluripotency in mouse ESCs (mESCs); but we report that hESCs maintain their stemness on soft substrate of varying stiffness. Our findings revealed that on soft substrate hESCs express pluripotency markers and does not undergo substrate-mediated differentiation. Interestingly we show that hESCs maintained basal level of YAP expression for cell survival and proliferation, but YAP expression does not correlate directly with pluripotency in hESCs. To summarize, our results show that hESCs retain their stemness on soft substrate despite downregulation of YAP.
      PubDate: 2022-06-28
       
  • PSMB2 knockdown suppressed proteasome activity and cell proliferation,
           promoted apoptosis, and blocked NRF1 activation in gastric cancer cells

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      Abstract: Abstract Proteasome 20S Subunit Beta 2 (PSMB2) has been suggested to play several roles in cancer. However, the role of PSMB2 and its underlying mechanisms in gastric cancer have not been studied. In this study, qRT-PCR was employed to detect the expression of genes that encode for 26 s proteasome subunit proteins. PSMB2 expression and its prognostic ability were assessed by collecting patient tissue samples and reviewing the TCGA and Kaplan–Meier Plotter databases. Immunofluorescence and western blotting experiments were performed to evaluate the expression of PSMB2 in human gastric cancer cells and normal gastric epithelial cells. Subsequently, PSMB2 was knocked down in HGC-27 and SNU-1 cells and overexpressed in N-87 and AGS cells. Proteasome activity assays, 5-Ethynyl-2′-deoxyuridine staining, and TUNEL assays were used to assess proteasome activity, cell proliferation, and apoptosis. Tumor xenograft assays were conducted to evaluate PSMB2 function in vivo. Our results showed that a total of 8 genes encoding for the 26 s proteasome subunit protein were highly expressed in a variety of gastric cancer cells. Next, PSMB2 was selected as the focus of subsequent studies which showed that PSMB2 was highly expressed in samples of gastric cancer tissue. Furthermore, a review of the TCGA database revealed that a high level of PSMB2 expression was associated with a poor clinical prognosis. Our results indicated that PSMB2 overexpression promoted proteasome activity, cell proliferation, and suppressed the apoptosis of gastric cancer cells, while those effects were reversed by treatment with a proteasome inhibitor (MG132). In contrast, PSMB2 knockdown produced the opposite effects and also blocked NRF1 activation. Moreover, PSMB2 knockdown inhibited tumor growth in vivo, decreased PSMB2 expression and cell proliferation, and promoted apoptosis in tumor tissues. Our findings revealed the role played by PSMB2 in gastric cancer and suggest PSMB2 as a new target molecule for use in diagnosing and treating gastric cancer.
      PubDate: 2022-06-27
       
  • MicroRNA-106b-5p (miR-106b-5p) suppresses the proliferation and metastasis
           of cervical cancer cells via down-regulating fibroblast growth factor 4
           (FGF4) expression

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      Abstract: Abstract This study aims to investigate the function and mechanism of microRNA-106b-5p (miR-106b-5p) in cervical cancer (CC). Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to determine miR-106b-5p expression in CC tissues and normal gastric tissues. Cell counting kit-8 (CCK-8) and colony formation assays were used to analyze the regulatory effects of miR-106b-5p on CC cells’ proliferative ability. Wound healing and Transwell assays were conducted to detect the effects of miR-106b-5p on cell migration and invasion. Besides, TargetScan was used to predict the potential target genes of miR-106b-5p. The interaction between miR-106b-5p and fibroblast growth factor 4 (FGF4) was proved by qRT-PCR, Western blot, and dual-luciferase reporter gene assay. MiR-106b-5p expression was down-regulated in CC tissues compared to non-tumorous tissues. The expression of miR-106b-5p was associated with the lymphatic node metastasis, FIGO stage and differentiation of CC. Functional assays revealed that miR-106b-5p overexpression suppressed CC cell proliferation, migration and invasion while miR-106b-5p inhibitor had the opposite effects. In addition, FGF4 was identified as a target gene of miR-106b-5p, and FGF could be negatively regulated by miR-106b-5p. MiR-106b-5p may serve as a tumor suppressor in CC, which can inhibit CC growth and metastasis by down-regulating FGF4 expression.
      PubDate: 2022-06-06
       
  • Targeting RPL23 restores chemosensitivity of cisplatin-resistant ovarian
           carcinoma by inhibiting EMT

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      Abstract: Abstract Chemoresistance is the inevitable outcome of chemotherapy for epithelial ovarian carcinoma (EOC), and its mechanism is still not fully understood. This study explored the role of ribosomal protein L23 (RPL23) in cisplatin resistance of EOC. WGCNA based on TCGA and GEO was used to screen and analyze target genes related to EOC chemotherapy sensitivity. Clinical samples of cisplatin resistance were collected to detect the expression of target genes. Cisplatin resistance was induced in EOC cell lines A2780 and SKOV3. The cell abilities of invasion, migration and adhesion were observed. Western blotting was used to detect protein expressions. Bioinformatics analysis showed that RPL23 may be related to EOC chemotherapy sensitivity, and was highly expressed in clinical samples and cell lines of cisplatin-resistant. After A2780 and SKOV3 were resistant to cisplatin, the inhibitory abilities of therapeutic dose of cisplatin on their invasion, migration and adhesion were significantly attenuated, and N-cadherin and vimentin were significantly up-regulated while E-cadherin was significantly down-regulated. However, above phenomena were significantly reversed after RPL23 knockdown. Taken together, the overexpressed RPL23 may lead to platinum resistance by inducing epithelial-mesenchymal transition (EMT) in EOC. Targeting knockdown RPL23 would restore the sensitivity of EOC cells to cisplatin by inhibiting EMT, suggesting that RPL23 is a potential therapeutic target for EOC after platinum resistance.
      PubDate: 2022-05-13
       
  • The secretome of microglia induced by IL-4 of IFN-γ differently regulate
           proliferation, differentiation and survival of adult neural
           stem/progenitor cell by targeting the PI3K-Akt pathway

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      Abstract: Abstract Microglia has been reported to be able to regulate the proliferation, differentiation and survival of adult neural stem/progenitor cells (NSPCs) by modulating the microenvironment, which results in different consequences of adult neurogenesis. However, whether the microglial activation is beneficial or harmful to NSPCs is still controversial because of the complexity and variability of microglial activation phenotypes. In this study, we systematically explored the activation phenotypes of IFN-γ- or IL-4-induced microglia at different time after stimulation, and investigated the effects of the secretome of different phenotype of microglia on the process of proliferation, differentiation and survival of NSPCs. Moreover, the possible molecular pathways of secretory influence on NSPCS were further explored using western blotting. The result showed that IFN-γ and IL-4 differently regulate microglial phenotypes, IL-4 induced a M2-like phenotype, while IFN-γ induced a M1-like phenotype. These phenotypes of microglia can only be maintained for 24 h after removal of IFN-γ or IL-4 intervention. The secretome from IFN-γ- or IL-4-induced microglia also had opposite effects on NSPCs proliferation, differentiation and survival. The secretome from the IL-4-treated microglia promoted NSPCs proliferation, survival and differentiation into neurons and oligodendrocytes, while factors secreted by the INF-γ-treated microglia stimulated the NSPCs differentiation into astrocyte, inhibited the neurogenesis and oligodendrogliogenesis, and induced NSPCs apoptosis. Furthermore, the PI3K-Akt pathway mediates the effects of the secretome from IFN-γ- or IL-4-induced microglia on NSPC proliferation, differentiation, and survival. In conclusion, our results suggested that the secretome of microglia induced by IL-4 of IFN-γ differently regulate proliferation, differentiation and survival of adult neural stem/progenitor cell by targeting the PI3K-Akt pathway. These findings will help further study the biological mechanism of microglia regulating neurogenesis, and provide a therapeutic strategy for neurological diseases by regulating microglial phenotypes to affect neurogenesis.
      PubDate: 2022-04-24
       
  • Static magnetic field regulates proliferation, migration, and
           differentiation of human dental pulp stem cells by MAPK pathway

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      Abstract: Abstract Magnetic materials are now commonly used in dental clinics. These materials generally produce a static magnetic field (SMF). While it is known that SMF can affect cells’ behaviors such as proliferation, migration, and differentiation, the mechanisms underlying these effects are still unclear. Our study investigates the role of the mitogen-activated protein (MAP) kinase pathway in SMF-induced proliferation, migration, osteogenic/odontogenic differentiation, and mineralization in human dental pulp stem cells (DPSCs). Human DPSCs were exposed to SMF of 1 mT and the phosphorylated MAP kinases were detected by Western blot analysis. Three MAP kinases inhibitors were pre-cultured with DPSCs and exposed to SMF for 24 h. Cell viability was analyzed using Cell Counting Kit-8. Cell migration was tested by a wound healing assay. Osteogenic/odontogenic differentiation was detected by ALP staining assay, ALP and DSPP Western blot analysis. Mineralization was studied by alizarin red staining analysis. SMF activated phosphorylation of c-Jun N-terminal kinase (JNK), P38 and extracellular signal-regulated kinase (ERK). The inhibition of JNK, P38, and ERK signaling decreased SMF-induced proliferation and migration. ERK and P38 play more important roles in SMF-induced ALP staining and protein expression. JNK was vital for SMF-induced DSPP expression. JNK, P38, and ERK all involved in SMF-mediated mineralization. Our study demonstrated that the MAPK pathway regulated SMF-induced proliferation, migration, osteogenic/odontogenic differentiation, and mineralization in human DPSCs.
      PubDate: 2022-04-20
      DOI: 10.1007/s10616-022-00533-3
       
  • ECRG4 acts as a tumor suppressor in nasopharyngeal carcinoma by
           suppressing the AKT/GSK3β/β-catenin signaling pathway

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      Abstract: Abstract Nasopharyngeal carcinoma (NPC) is a malignant tumor with a poor prognosis. Studies have shown that esophageal carcinoma related gene 4 (ECRG4) is hypermethylated and significantly downregulated in NPC tissues. However, the role of ECRG4 in NPC, and in particular the underlying molecular mechanism, is largely unclear. In this study, using immunohistochemical staining of ECRG4 in NPC and normal specimens, we confirmed that ECRG4 was downregulated in human NPC tissues. In addition, various biological and molecular studies were carried out and the results showed that ECRG4 exerted anticancer effect in NPC, including inhibiting cell growth, migration, and invasion of NPC cells in vitro. Moreover, restoring ECRG4 expression suppressed the in vivo tumorigenesis of CNE2 cells. ECRG4 inhibited AKT/GSK3β/β-catenin signaling, as well as the downstream targets of β-catenin. LiCl treatment, which reduced GSK3β phosphorylation and upregulated β-catenin expression, restored the invasive ability of ECRG4-overexpressing NPC cells. Furthermore, we showed that the DNA methylation inhibitor 5-aza-dC reduced ECRG4 methylation and the invasive ability of negative control cells, but not that of ECRG4-overexpressing cells, suggesting that the inhibitory effect of 5-aza-dC depends on low expression of ECRG4. Collectively, our results demonstrated that ECRG4 downregulation contributed to NPC growth and invasion by activating AKT/GSK3β/β-catenin signaling pathway. ECRG4 could be a promising therapeutic target for the treatment of NPC.
      PubDate: 2022-04-01
      DOI: 10.1007/s10616-022-00520-8
       
  • Age-related functional decline of human B cells

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      Abstract: Abstract This study aimed to investigate the changes in B cell functional decline and antigen sensitization with aging using two Epstein Barr virus (EBV)-immortalized human B cell lines, one from a 22-year-old man (EBV-B young) and the other from a 65-year-old man (EBV-B old). The activity of senescence-associated β-galactosidase, a marker of cellular senescence, was enhanced in the EBV-B old cells compared with EBV-B young cells. Moreover, the levels of p16, p21, IL-6, TNF-α, and TGF-β1, which are senescence-associated secretary phenotypes, were also increased in EBV-B old cells. In vitro immunization of EBV-B cells with β-lactoglobulin further showed that EBV-B old cells had a reduced cell population of naïve B cells than that of EBV-B young cells. Furthermore, HLA-DR expression, which is important for antigen presentation, was decreased in the EBV-B old cells. Comparative microarray analysis between EBV-B young and old cells also showed decreased expression of antibody genes, such as those of the heavy chain and light chain (κ chain). These results suggest that cellular senescence and decreased gene expression are responsible, at least in part, for the decline in B cell function and antigen sensitization capacity with aging, which ultimately impairs the function of the acquired immune system.
      PubDate: 2022-04-01
      DOI: 10.1007/s10616-021-00513-z
       
  • PBX1 attenuates 6-OHDA-induced oxidative stress and apoptosis and affects
           PINK1/PARKIN expression in dopaminergic neurons via FOXA1

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      Abstract: Abstract PBX1 expression has been found to be significantly reduced in nigrostriatal neurons of PD patients, but the effect of PBX1 on ROS and apoptosis in nigrostriatal dopamine neurons is not yet known. This paper aimed to explore whether PBX1 could be involved in the development of PD. The construction of the in vitro PD model was followed by the determination of PBX1 expression. Then, PBX1 was overexpressed to observe the changes in the cell viability, TH expression, oxidative stress and apoptosis of the model. The mitochondrial membrane potential analysis and detection of PINK1/parkin expression were also conducted. To observe whether FOXA1 was involved in the mechanism, its expression was measured, and its association with PBX1 was determined. Subsequently, FOXA1 was silenced to observe whether PBX1 did effects on dopaminergic neuron via FOXA1. PBX1 attenuates 6-OHDA-induced dopaminergic neuronal cell injury and oxidative stress, and apoptosis. Its overexpression ameliorates mitochondrial dysfunction in dopaminergic neurons and upregulates the expression of PINK1/parkin. PBX1 could combine with FOXA1 and affects 6-OHDA-induced dopaminergic neuronal damage and regulates PINK1/PARKIN expression via FOXA1. To conclude, PBX1 attenuates 6-OHDA-induced oxidative stress and apoptosis in dopaminergic neurons, and affected PINK1/PARKIN expression via FOXA1, which indicates the great potential of the PBX1 in prevention against PD.
      PubDate: 2022-04-01
      DOI: 10.1007/s10616-021-00518-8
       
  • Protective effects of liquiritin on polycystic ovary syndrome through
           modulating ovarian granulosa cell proliferation and apoptosis via
           miR-206/PI3K/AKT pathway

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      Abstract: Abstract Polycystic ovarian syndrome (PCOS) is a frequent metabolic disorder in premenopausal woman, featured with increased androgen, reduced ovulation and insulin resistance. An increasing number of reports have confirmed that microRNAs (miRNAs) play pivotal roles in PCOS. However, the diagnostic mechanisms of microRNA (miR)-206 in PCOS remain unclear. Liquiritin, extracted from Glycyrrhiza Radix, has multiple pharmacological activities in diseases, including PCOS. Our report was designed to explore whether liquiritin play a role in PCOS by regulating human ovarian granulosa cell-like KGN cells proliferation and apoptosis through miR-206/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, and to further elucidate the underlying molecular mechanisms. KGN cells were exposed to various concentration (0, 20, 40, 80 μM) of liquiritin for 48 h, cell proliferation and apoptosis were measured by 3-(45)-dimethylthiahiazo(-z-y1)-35-di-phenytetrazoliumromide (MTT) and flow cytometry analysis. Reverse transcription‑quantitative polymerase chain reaction was conducted to checked the levels of miR-206 in KGN cells. The protein expression levels of cleaved caspase3, caspase3, phosphorylated (p)-AKT and AKT were analyzed using Western blot assay. We found that liquiritin stimulation led to reduced viability and enhanced apoptotic KGN cells, which along with increased cleaved caspase3 and cleaved caspase3/caspase3 ratio. Moreover, liquiritin obviously reduced p-AKT expression and p-AKT/AKT ratio. MiR-206 was up-regulated in liquiritin-treated KGN cells, however, all these results were reversed by miR-206 inhibitor. In conclusion, our findings suggested that liquiritin exerted anti-proliferative and apoptosis-inducing roles in KGN cells via miR-206/PI3K/AKT pathway, suggesting that liquiritin may be an effective therapeutic target for PCOS treatment.
      PubDate: 2022-03-21
      DOI: 10.1007/s10616-022-00531-5
       
  • OCT4, SOX2 and NANOG co-regulate glycolysis and participate in somatic
           induced reprogramming

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      Abstract: Abstract OCT4, SOX2 and NANOG (OSN) are the key factors of cell reprogramming, which are involved in the maintenance of stem cell pluripotency. Recently, it has been found that glycolysis plays an important role in the process of somatic-cell-induced reprogramming; however, the synergistic effect of OSN on glycolysis has rarely been reported. In this study, chicken embryonic fibroblasts (CEF) was reprogrammed into induced pluripotent stem cells (iPSCs) by OCT4, SOX2, NANOG and LIN28 reprogramming strategy. RNA-seq showed that chicken iPSCs highly expressed pluripotent genes and the expression of the key genes of glycolysis, such as Hk1, Pfkp and Ldha, was also at a high level, while CEF was much lower. Glycolysis gene expression, glucose uptake and lactate production of CEF and iPSCs were also detected. The results showed that the glycolysis level of iPSCs was higher than that of CEF. ChIP-qPCR showed that SOX2 and NANOG transcription factors were significantly enriched in the promoter regions of Hk1, Pfkp and Ldha, while OCT4 was not. The above results indicated that OCT4, SOX2 and NANOG coordinately regulate glycolysis and participate in somatic-cell-induced reprogramming, thus setting a good foundation for further research on the molecular mechanism of somatic-cell-induced reprogramming.
      PubDate: 2022-03-17
      DOI: 10.1007/s10616-022-00530-6
       
  • Development of a novel feeding regime for large scale production of human
           umbilical cord mesenchymal stem/stromal cells

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      Abstract: Abstract Human umbilical cord mesenchymal stem/stromal cells (hUC-MSCs) have attracted significant research interests in regenerative medicine and cell-based therapies due to their minimally invasive isolation procedure, abundant availability, allogenic nature, improved proliferation capacity and tri-lineage differentiation potential. However, the challenge in harvesting a sufficient number of hUC-MSCs through conventional static culture for downstream application hinders the downstream clinical translation of hUC-MSCs. Hence, an alternative culture method that can facilitate large-scale expansion is highly desirable. Herein, we developed a microcarrier-based dynamic culture system to culture hUC-MSCs combined fed-batch mode with medium refreshment to decrease concentrations of metabolic wastes, improve nutrient supplement and reduce the amount of medium used for cell culture. Instead of refreshing medium based on the pre-determined frequency, the replacement and feeding of medium using the novel feeding regime were carried out based on consumption of nutrients (glucose and glutamine) and production of metabolic waste (lactate and ammonia) to maintain a balanced and benign culture microenvironment. The optimal process allowed over 20 folds increase of cell with a maximum cell density at (24.13 ± 0.59) × 105 cells/mL. In addition, no significant alteration of cell surface markers of hUC-MSCs derived from dynamic conditions was observed compared to static conditions. Impressively, over 99.8% of the cellular population showed the desired positive expression of CD73, CD90 and CD105, while less than 0.2% of the population showed undesired negative expression of CD34, CD45 and HLA-DR. More importantly, hUC-MSCs derived from our dynamic culture condition still maintained their trilineage differentiation capacity.
      PubDate: 2022-03-10
      DOI: 10.1007/s10616-022-00523-5
       
  • Protective effects of lidocaine on polycystic ovary syndrome through
           modulating ovarian granulosa cell physiology via PI3K/AKT/mTOR pathway

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      Abstract: Abstract Polycystic ovary syndrome (PCOS) is a common endocrine condition in women that causes adverse reproductive and metabolic effects. PCOS is a heterogeneous disorder and its pathogenesis is affected by different factors. Thus, the criteria for diagnosing PCOS, disease and availability of treatment options vary widely across different countries. Lidocaine has been proven to inhibit the proliferation of a variety of cancer cell types, and can be used alone or in combination with other drugs for the treatment of numerous types of disease. The present study aimed to determine whether lidocaine was able to reduce human ovarian granulosa cell tumor cell line KGN cell proliferation and provide a novel insight into potential therapeutic strategies for PCOS. KGN cells were treated alone with lidocaine at different concentrations, or with lidocaine and insulin-like growth factor-1 (IGF-1; a phosphoinositide 3-kinase (PI3K)/Protein kinase B (AKT) signaling pathway agonist) in combination for 48 h. The proliferative ability of KGN cells was detected using an 3-(45)-dimethylthiahiazo (-z-y1)-35-di- phenytetrazoliumromide (MTT) assay, and cell apoptosis was detected using flow cytometry. The expression levels of proteins and mRNAs were measured using western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), respectively. The results of the present study revealed that lidocaine significantly suppressed KGN cell proliferation and increased apoptosis. Lidocaine significantly downregulated the protein expression levels of phosphorylated (p)-AKT and p-mTOR, but had no effect on their transcriptional levels. Treatment with IGF-1, could reverse the lidocaine-induced abnormal expression of PI3K/AKT signaling pathway-related proteins. Moreover, treatment with IGF-1 could reverse all the effects of lidocaine on KGN cells. In conclusion, the findings of the present study indicated that lidocaine may inhibit KGN cell proliferation and induce apoptosis by inhibiting the activation of the PI3K/AKT/mTOR signaling pathway. These results revealed the potential inhibitory effect of lidocaine on the proliferation of KGN cells and its underlying mechanism of action, providing a novel insight into potential therapeutic strategies for PCOS.
      PubDate: 2022-02-24
      DOI: 10.1007/s10616-022-00528-0
       
  • Surface coating materials regulates the attachment and differentiation of
           mouse embryonic stem cell derived embryoid bodies into mesoderm at culture
           conditions

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      Abstract: Pluripotent stem cells as a promising cell source with unlimited proliferation and differentiation capacity hold great promise for cell-based therapies in regenerative medicine. Establishment of appropriate culture conditions might enable the control of cellular fate decision in cell culture. Transfer of three-dimensional (3D) embryoid bodies to two-dimensional (2D) monolayer culture systems for initiation of cell differentiation and specialization requires an adaptation of cells which can be managed by extracellular matrix (ECM) materials. Here we compare the characteristics of four different cell culture coating materials and their effect on attachment and differentiation of cells spreading from mouse embryonic stem cell (mESC) derived embryoid bodies (EBs) in mesoderm inducing culture conditions. Atomic force microscope (AFM) and scanning electron microscope (SEM) analysis along with Water Contact Angle technique were used to analyze physical properties of ECM materials and to evaluate cellular behavior on surfaces. Cell migration and differentiation were performed initially by using mesoderm inducing culture conditions and then three germ layer specification conditions. We investigated properties of coating materials such as roughness and wettability control cell attachment, migration and differentiation of mESCs. Matrigel-Gelatin combination is suitable for cell attachment and migration of cells spreading from 3D EBs followed by transfer onto coated surfaces. Matrigel-Gelatin coating enhanced differentiation of cells into mesoderm like cells via EMT process. Our data demonstrated that the Matrigel-Gelatin combination as a cell culture coating matrix might serve as a suitable platform to transfer EBs for differentiation and might influence pluripotent stem cell fate decision into mesoderm and further mesoderm derivative cell populations. Graphical abstract
      PubDate: 2022-02-22
      DOI: 10.1007/s10616-022-00529-z
       
  • Th22/IL-22 mediates the progression of HBV-related hepatocellular
           carcinoma via STAT3

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      Abstract: Abstract T helper cell 22 are abundant in Hepatitis B Virus-related hepatocellular carcinoma tissue, and the main cytokine interleukin 22 produced by Th22 cells is closely related to the initiation and development of HCC. Understanding the role of Th22/IL-22 in the progression of HBV-related HCC will facilitate new therapeutic development. Th22 cells were isolated from peripheral blood of healthy donors and co-cultured with HBV positive HepG2.2.15 cells. IL-22 secretion and HepG2.2.15 cell proliferation and apoptosis were monitored. Expressions of p-STAT3, Cyclin D1, Bcl-2, and cleaved caspase 3 were detected by Western blot analysis. Th22 cells significantly promoted the proliferation and inhibited the apoptosis of HepG2.2.15 cells; up-regulated expression of p-STAT3, Cyclin D1 and Bcl-2, and down-regulated cleaved caspase 3 in HepG2.2.15 cells. These effects were significantly attenuated when IL-22 and STAT3 was knockdown in Th22 and HepG2.2.15 cells, respectively. Our data suggests that HBV induces host Th22 cells to overexpress IL-22, which in turn triggers over-activation of STAT3 and its downstream signaling proteins to promote HCC progression.
      PubDate: 2022-02-22
      DOI: 10.1007/s10616-021-00517-9
       
  • Differential in vitro anti-leukemic activity of resveratrol combined with
           serine palmitoyltransferase inhibitor myriocin in FMS-like tyrosine kinase
           3-internal tandem duplication (FLT3-ITD) carrying AML cells

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      Abstract: Abstract Treatment of FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) AML is restricted due to toxicity, drug resistance and relapse eventhough targeted therapies are clinically available. Resveratrol with its multi-targeted nature is a promising chemopreventive remaining limitedly studied in FLT3-ITD AML regarding to ceramide metabolism. Here, its cytotoxic, cytostatic and apoptotic effects are investigated in combination with serine palmitoyltransferase (SPT), the first enzyme of de novo pathway of ceramide production, inhibitor myriocin on MOLM-13 and MV4-11 cells. We assessed dose-dependent cell viability, flow cytometric cell death and cell cycle profiles of resveratrol in combination with myriocin by MTT assay, annexin-V/PI staining and PI staining respectively. Resveratrol’s dose-dependent effect on SPT protein expression was also checked by western blot. Resveratrol decreased cell viability in a dose- dependent manner whereas myriocin did not affect cell proliferation effectively in both cell lines after 48h treatments. Although resveratrol induced both apoptosis and a significant S phase arrest in MV4-11 cells, it triggered apoptosis and non-significant S phase accumulation in MOLM-13 cells. Co-administrations reduced cell viability. Increased cytotoxic effect of co-treatments was further proved mechanistically through induction of apoptosis via phosphatidylserine relocalization. The cell cycle alteration in co-treatment was significant with an S phase arrest in MV4-11 cells, however, it was not effective on cell cycle progression of MOLM-13 cells. Resveratrol also increased SPT expression. Overall, modulation of SPT together with resveratrol might be the possible explanation for resveratrol’s action. It could be an integrative medicine for FLT3-ITD AML after investigating its detailed mechanism of action in relation to de novo pathway of ceramide production.
      PubDate: 2022-02-14
      DOI: 10.1007/s10616-022-00527-1
       
  • Perilla pomace obtained from four different varieties have different
           levels and types of polyphenols and anti-allergic activity

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      Abstract: Abstract Perilla frutescens (L.) Britton var. frutescens (egoma in Japan) is a traditional oilseed that has several varieties with different photoperiod responses. Although egoma pomace, industrial waste produced during oil extraction, is a rich source of macro- and micro-nutrients such as protein, fiber, minerals, and polyphenols, it has not yet been used for purposes other than livestock feeding. To find out a better use of perilla pomace and its function, we selected four varieties of egoma originating from different regions with different photoperiod responses: two varieties were from Japan, which are broadly cultivated for oilseed and are highly sensitive to light and temperature. The other two varieties from Nepal, which are tolerant to low light and low temperature. Rosmarinic acid-3-O-glucoside, rosmarinic acid, and apigenin-7-O-glucoside were detected as the main polyphenolic constituents in every variety, while apigenin and luteolin were present only in perilla pomace from Japan. In IgE-sensitized RBL-2H3 cells, polyphenols derived from two varieties of Japan suppressed degranulation of mast cells, but those derived from the two varieties of Nepal did not, indicating that apigenin and luteolin may be in part responsible for the anti-allergic response. In addition, it was found that proteins involved in the degranulation signaling pathway, such as PLCγ2, Syk, and Akt, were less phosphorylated in cells treated with the egoma pomace extracts of Japanese origin. Taken together, pomace from egoma varieties derived from different regions may differently modulate allergic response in part due to the difference in polyphenol composition and may be applied to develop nutraceuticals and functional foods fortified with anti-allergic properties.
      PubDate: 2022-02-11
      DOI: 10.1007/s10616-022-00522-6
       
  • Gene delivery in adherent and suspension cells using the combined physical
           methods

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      Abstract: Abstract Physical methods are widely utilized to deliver nucleic acids into cells such as electro-transfection or heat shock. An efficient gene electro-transfection requires the best conditions including voltage, the pulse length or number, buffer, incubation time and DNA form. In this study, the delivery of pEGFP-N1 vector into two adherent cell lines (HEK-293 T and COS-7) with the same origin (epithelial cells), and also mouse bone marrow-derived dendritic cells (DCs) was evaluated using electroporation under different conditions alone and along with heat treatment. Our data showed that the highest green fluorescent protein (GFP) expression in HEK-293 T and COS-7 cells was observed in serum-free RPMI cell culture medium as electroporation buffer, voltage (200 V), the pulse number (2), the pulse length (15 ms), the circular form of DNA, and 48 h after electro-transfection. In addition, the highest GFP expression in DCs was detected in serum-free RPMI, voltage (300 V), the pulse number (1), the pulse length (5 ms), and 48 h after electro-transfection. The use of sucrose as electroporation buffer, the pulse number (2), and the pulse length (25 ms) led to further cytotoxicity and lower transfection in HEK293T and COS-7 cells than other conditions. Moreover, the high voltage (700 V) increased the cell cytotoxicity, and decreased electro-transfection efficiency in DCs. On the other hand, the best conditions of electroporation along with heat treatment could significantly augment the transfection efficiency in all the cells. These data will be useful for gene delivery in other cells with the same properties using physical methods.
      PubDate: 2022-02-03
      DOI: 10.1007/s10616-022-00524-4
       
  • Prdm12 regulates inhibitory neuron differentiation in mouse embryonal
           carcinoma cells

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      Abstract: Abstract The epigenetic regulatory system significant influences the fate determination of cells during developmental processes. Prdm12 is a transcriptional regulator that modulates gene expression epigenetically. The Prdm12 gene has been shown to be expressed in neural tissues, specifically during development, but its detailed function is not fully understood. This study investigated the function of the Prdm12 gene in P19 mouse embryonic tumor cells as a model for neural differentiation. A decrease in the expression of neuron-specific genes and the alterations of dendrites and axons morphology was confirmed in Prdm12-knockout P19 cells. In addition, almost no astrocytes were generated in Prdm12-knockout P19 cells. Comprehensive gene expression analysis revealed that there was a reduction in the expression of the inhibitory neuron-specific genes Gad1/2 and Glyt2, but not the excitatory neuron-specific gene VGLUT2, in Prdm12-knockout P19 cells. Furthermore, the expression of inhibitory neuron-related factors, Ptf1a, Dbx1, and Gsx1/2, decreased in Prdm12-knockout P19 cells. Gene expression analysis also revealed that the Ptf1a, Hic1, and Foxa1 genes were candidate targets of Prdm12 during neurogenesis. These results suggest that Prdm12 regulates the differentiation of inhibitory neurons and astrocytes by controlling the expression of these genes during the neural differentiation of P19 cells.
      PubDate: 2022-02-02
      DOI: 10.1007/s10616-022-00519-1
       
 
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