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Cell Biochemistry and Biophysics
Journal Prestige (SJR): 0.581  Citation Impact (citeScore): 2 Number of Followers: 9  Hybrid journal (It can contain Open Access articles)ISSN (Print) 1559-0283 - ISSN (Online) 1085-9195 Published by Springer-Verlag  [2468 journals]
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- Correction: ER Stress Decreases Gene Expression Of Transmembrane Protein
117 Via Activation of PKR-like ER Kinase-
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PubDate: 2023-12-01
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- Editorial Expression of Concern: Induction of Human Bone Marrow
Mesenchymal Stem Cells Differentiation into Neural-Like Cells Using
Cerebrospinal Fluid-
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PubDate: 2023-12-01
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- Alcohol Intake Provoked Cardiomyocyte Apoptosis Via Activating
Calcium-Sensing Receptor and Increasing Endoplasmic Reticulum Stress and
Cytosolic [Ca2+]i-
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Abstract: Background Cardiomyocyte apoptosis plays an important role in alcoholic cardiac injury. However, the association between calcium-sensing receptor (CaSR) and alcohol-induced cardiomyocyte apoptosis remain unclear. Therefore, we investigated the role and its moleculer mechanism of CaSR in rat cardiomyocyte apoptosis induced by alcohol. Methods Alcohol-induced cardiomyocyte apoptosis in vivo and in vitro model of rats were applied in this study. The expression of CaSR, endoplasmic reticulum stress markers and apoptosis were tested by immunohistological staining, western blot, TUNEL and flow cytometry, respectively. [Ca2+]i were detected by confocal laser scanning microscopy. Results Compared with the control group, alcohol intake (AI) led to abnormal arrangements of cardiomyocytes and obvious increase of myocardial apoptosis. Moreover, AI also significantly upregulated protein expression of CaSR, GRP94, caspase-12 and CHOP. Alcohol induced apoptosis of cultured cardiomyocytes of rats in a dose-dependent way. Activation of CaSR markedly enhanced cardiomyocyte apoptosis and ERS induced by alcohol, ERS inducer also significantly increased cardiomyocyte apoptosis without activating CaSR. Furthermore, GdCl3 augmented alcohol-induced increase of [Ca2+]i in cardiomyocytes, which was attenuated by NPS2390 but not 4-PBA pre-treatment. Conclusions Alcohol could induce cardiomyocyte apoptosis in rats in vivo and in vitro, which was mediated probably via activating CaSR, and then ERS and the increase of the cytosolic [Ca2+]i. This provides a potential target for preventing cardiomyocyte apoptosis and cardiomyopathy induced by alochol.
PubDate: 2023-12-01
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- Inhibitors Targeting the F-BOX Proteins
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Abstract: F-box proteins are involved in multiple cellular processes through ubiquitylation and consequent degradation of targeted substrates. Any significant mutation in F-box protein-mediated proteolysis can cause human malformations. The various cellular processes F-box proteins involved include cell proliferation, apoptosis, invasion, angiogenesis, and metastasis. To target F-box proteins and their associated signaling pathways for cancer treatment, researchers have developed thousands of F-box inhibitors. The most advanced inhibitor of FBW7, NVD-BK M120, is a powerful P13 kinase inhibitor that has been proven to bring about apoptosis in cancerous human lung cells by disrupting levels of the protein known as MCL1. Moreover, F-box Inhibitors have demonstrated their efficacy for treating certain cancers through targeting particular mutated proteins. This paper explores the key studies on how F-box proteins act and their contribution to malignancy development, which fabricates an in-depth perception of inhibitors targeting the F-box proteins and their signaling pathways that eventually isolate the most promising approach to anti-cancer treatments.
PubDate: 2023-12-01
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- Impeding DNA Polymerase β Activity by Oleic Acid to Inhibit Base Excision
Repair and Induce Mitochondrial Dysfunction in Hepatic Cells-
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Abstract: Free fatty acids (FFAs) hepatic accumulation and the resulting oxidative stress contribute to several chronic liver diseases including nonalcoholic steatohepatitis. However, the underlying pathological mechanisms remain unclear. In this study, we propose a novel mechanism whereby the toxicity of FFAs detrimentally affects DNA repair activity. Specifically, we have discovered that oleic acid (OA), a prominent dietary free fatty acid, inhibits the activity of DNA polymerase β (Pol β), a crucial enzyme involved in base excision repair (BER), by actively competing with 2′-deoxycytidine-5′-triphosphate. Consequently, OA hinders the efficiency of BER, leading to the accumulation of DNA damage in hepatocytes overloaded with FFAs. Additionally, the excessive presence of both OA and palmitic acid (PA) lead to mitochondrial dysfunction in hepatocytes. These findings suggest that the accumulation of FFAs hampers Pol β activity and contributes to mitochondrial dysfunction, shedding light on potential pathogenic mechanisms underlying FFAs-related diseases.
PubDate: 2023-12-01
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- Investigation of Simultaneous and Sequential Cooperative Homotropic
Inhibitor Binding to the Catalytic Chamber of SARS-CoV-2 RNA-dependent RNA
Polymerase (RdRp)-
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Abstract: In our previous report, the unique architecture of the catalytic chamber of the SARS-CoV-2 RNA-dependent RNA polymerase (RdRp), which harbours two distinctive binding sites, was fully characterized at molecular level. The significant differences in the two binding sites BS1 and BS2 in terms of binding pockets motif, as well as the preferential affinities of eight anti-viral drugs to each of the two binding sites were described. Recent Cryogenic Electron Microscopy (Cryo-EM) studies on the RdRp revealed that two suramin molecules, a SARS-CoV-2 inhibitor, bind to RdRp in two different sites with distinctive interaction landscape. Here, we provide the first account of investigating the combined inhibitor binding to both binding sites, and whether the binding of two inhibitors molecules concurrently is “Cooperative binding” or not. It should be noted that the binding of inhibitors to different sites do not necessary constitute mutually independent events, therefore, we investigated two scenarios to better understand cooperativity: simultaneous binding and sequential binding. It has been demonstrated by binding free energy calculations (MM/PBSA) and piecewise linear potential (PLP) interaction energy analysis that the co-binding of two suramin molecules is not cooperative in nature; rather, when compared to individual binding, both molecules adversely affect one another’s binding affinities. This observation appeared to be primarily due to RdRp’s rigidity, which prevented both ligands from fitting comfortably within the catalytic chamber. Instead, the suramin molecules showed a tendency to change their orientation within the binding pockets in order to maintain their binding to the protein, but at the expense of the ligand internal energies. Although co-binding resulted in the loss of several important key interactions, a few interactions were conserved, and these appear to be crucial in preserving the binding of ligands in the active site. The structural and mechanistic details of this study will be useful for future research on creating and developing RdRp inhibitors against SARS-CoV-2.
PubDate: 2023-12-01
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- Infliximab Ameliorates Methotrexate-Induced Nephrotoxicity in Experimental
Rat Model: Impact on Oxidative Stress, Mitochondrial Biogenesis, Apoptotic
and Autophagic Machineries-
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Abstract: Accumulating data confirms that Methotrexate (MTX), a well-known immunosuppressive and anticancer drug, causes nephrotoxicity. Infliximab (INF), the inhibitor of tumor necrosis factor-alpha (TNF-α), was proven to have anti-inflammatory properties. Thus, it may have potential in preventing MTX-induced nephrotoxicity. Therefore, this study aimed to inspect the prospective nephroprotective effect of INF on MTX-induced rat nephrotoxicity through investigating the possible molecular mechanisms, including its interference with different death routes, oxidative stress as well as mitochondrial biogenesis. Rats received an INF intraperitoneal single dose of 7 mg/kg 72 h prior to a single 20 mg/kg MTX injection. MTX nephrotoxicity was demonstrated by significantly increased serum levels of the renal indicators urea and creatinine as well as renal inflammatory markers TNF-α and Interleukin-6 (IL-6) and the renal oxidative stress marker malondialdehyde (MDA), while renal antioxidant enzyme superoxide dismutase (SOD) was significantly decreased compared to control. INF injection prior to MTX markedly reversed these MTX-induced effects. Besides, MTX impaired mitochondrial biogenesis, while INF attenuated this impairment, as indicated by increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Finally, MTX triggered apoptotic and autophagic cascades in renal tissues as evidenced by reduced anti-apoptotic Bcl-2 protein expression as well as elevated expression of the pro-apoptotic protein Bax and both key regulators of autophagy; beclin-1 and LC-3, whereas INF pretreatment counteracted these apoptotic and autophagic effects of MTX. Summarily, these results suggest that INF provides protection against MTX-induced nephrotoxicity which could be elucidated by its antioxidant, anti-inflammatory, anti-apoptotic and anti-autophagic effects as well as upregulating mitochondrial biogenesis.
PubDate: 2023-12-01
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- Disruption of Bioenergetics in the Intestine of Wistar Rats Caused by
Hydrogen Sulfide and Thiosulfate: A Potential Mechanism of Chronic
Hemorrhagic Diarrhea in Ethylmalonic Encephalopathy-
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Abstract: Ethylmalonic encephalopathy (EE) is a severe inherited metabolic disorder that causes tissue accumulation of hydrogen sulfide (sulfide) and thiosulfate in patients. Although symptoms are predominantly neurological, chronic hemorrhagic diarrhea associated with intestinal mucosa abnormalities is also commonly observed. Considering that the pathophysiology of intestinal alterations in EE is virtually unknown and that sulfide and thiosulfate are highly reactive molecules, the effects of these metabolites were investigated on bioenergetic production and transfer in the intestine of rats. We observed that sulfide reduced NADH- and FADH2-linked mitochondrial respiration in the intestine, which was avoided by reduced glutathione (GSH) but not by melatonin. Thiosulfate did not change respiration. Moreover, both metabolites markedly reduced the activity of total, cytosolic and mitochondrial isoforms of creatine kinase (CK) in rat intestine. Noteworthy, the addition of GSH but not melatonin, apocynin, and Trolox (hydrosoluble vitamin E) prevented the change in the activities of total CK and its isoforms caused by sulfide and thiosulfate, suggesting a direct protein modification on CK structure by these metabolites. Sulfide further increased thiol content in the intestine, suggesting a modulation in the redox state of these groups. Finally, sulfide and thiosulfate decreased the viability of Caco-2 intestinal cells. Our data suggest that bioenergetic impairment caused by sulfide and thiosulfate is a mechanism involved in the gastrointestinal abnormalities found in EE.
PubDate: 2023-12-01
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- Macrophages Serve as Bidirectional Regulators and Potential Therapeutic
Targets for Liver Fibrosis-
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Abstract: Liver fibrosis is a dynamic pathological process in which the structure and function of the liver abnormally change due to long-term complex inflammatory reactions and chronic liver injury caused by multiple internal and external factors. Previous studies believed that the activation of hepatic stellate cells is a critical part of the occurrence and development of liver fibrosis. However, an increasing number of studies have indicated that the macrophage plays an important role as a central regulator in liver fibrosis, and it directly affects the development and recovery of liver fibrosis. Studies of macrophages and liver fibrosis in the recent 10 years will be reviewed in this paper. This review will not only clarify the molecular mechanism of liver fibrosis regulated by macrophages but also provide new strategies and methods for ameliorating and treating liver fibrosis.
PubDate: 2023-12-01
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- Inhibited Expression of NLRP12 Promotes the Development of Triple-Negative
Breast Cancer by Activating the NF-κB Pathway-
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Abstract: NLRP12 can affect the progression of different diseases, including hepatocellular carcinoma. However, no report on triple-negative breast cancer (TNBC) has been found. Thus, this study aimed to explore the role of NLRP12 in TNBC. In our study, immunohistochemistry, real-time quantitative PCR (qPCR), and Western blot assays were used to evaluate NLRP12 expression in TNBC tissues and cells. Then, NLRP12 lentivirus was constructed and infected into MDA-MB-231 and MDA-MB-157 cells with or without PTD-p65-P1 treatment. Next, cells were collected for cell function detection using the following procedures: colony formation assay for proliferation, Transwell for migration and invasion, and Western blot for NF-κB and MAPK pathway-associated proteins. Finally, a xenograft mouse model was applied; the tumor volume and weight were determined, and NLRP12, p-IκBb-α, and p-IκBb-α expressions were evaluated using qPCR and Western blot. Results indicated that NLRP12 was lowly expressed in TNBC tissues and cells. The inhibition of NLRP12 could induce the proliferation, migration, and invasion of TNBC cells, which also could be reversed by inhibiting the NF-κB pathway (PTD-p65-P1). Moreover, silencing of NLRP12 could upregulate p-IκBb-α, while IκBb-α, p-ERK, ERK, p-p38, p38, p-JNK, and JNK expressions remained unchanged, thereby indicating that only the NF-κB pathway could be activated by NLRP12 silencing. Furthermore, the xenograft mouse model confirmed the abovementioned findings. Therefore, the low expression of NLRP12 promoted the proliferation, migration, and invasion in TNBC cells by activating the NF-κB pathway. This study might provide insights into TNBC therapy.
PubDate: 2023-12-01
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- Sodium Glucose Transporter-2 Inhibitors (SGLT2Is)-TLRs Axis Modulates
Diabetes-
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Abstract: Diabetes affects millions of people worldwide and is mainly associated with impaired insulin function. To date, various oral anti-diabetic drugs have been developed, of which, the sodium glucose transporter-2 inhibitors (SGLT2Is) are of the most recent classes that have been introduced. They differ from other classes in terms of their novel mechanism of actions and unique beneficial effects rather than just lowering glucose levels. SGLT2Is can protect body against cardiovascular events and kidney diseases even in non-diabetic individuals. SGLT2Is participate in immune cell activation, oxidative stress reduction, and inflammation mediation, thereby, moderating diabetic complications. In addition, toll like receptors (TLRs) are the intermediators of the immune system and inflammatory process, thus it’s believed to play crucial roles in diabetic complications, particularly the ones that are related to inflammatory reactions. SGLT2Is are also effective against diabetic complications via their anti-inflammatory and oxidative properties. Given the anti-inflammatory properties of TLRs and SGLT2Is, this review investigates how SGLT2Is can affect the TLR pathway, and whether this could be favorable toward diabetes.
PubDate: 2023-12-01
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- D348N Mutation of BFSP1 Gene in Congenital Cataract: it Does Matter
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Abstract: Beaded filament structural protein 1 (BFSP1) gene plays important role in the development of congenital cataract. We aimed to investigate and analyze the molecular mechanism of congenital cataract caused by D348N mutation of BFSP1 gene, and to provide evidence for the intervention of congenital cataract. BFSP1 and CP49 genes were cloned, wild type and mutant expression plasmids of BFSP1 were constructed and transfected into 293T cells. The BFSP1 wild type and mutant (D348N) gene sequence (NM_001195) were constructed into pEGFP-N1 vector by the restriction site NheI/KpnI. The effect of mutation on cell proliferation and apoptosis was analyzed. There was no significant change between the expression site of BFSP1 D348N mutation and the wild type. The expression of BFSP1 protein in wild group was higher than that in mutant group. CCK8 detection showed that the proliferation ability of 293T cells in mutant group was weaker than that in BFSP1 group. The mutation led to an increase in apoptosis. BFSP1 mutation significantly decreases the expression of BFSP1 protein, weakened the ability of cell proliferation and increased apoptosis. BFSP1 D348N mutation may be closely associated with congenital cataract and is of great significance to the investigations of the mechanism and intervention of congenital cataract.
PubDate: 2023-12-01
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- Matrix Stiffness Regulated Endoplasmic Reticulum Stress-mediated Apoptosis
of Osteosarcoma Cell through Ras Signal Cascades-
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Abstract: The modulating effects of matrix stiffness on spreading and apoptosis of tumor cells have been well recognized. Nevertheless, the detail road map leading to the apoptosis and the underlying mechanisms governing the cell apoptosis have remained to be elucidated. To this aim, we provided a tunable elastic hydrogel matrix that promoted cell adhesion by modifying the surface of polyacrylamide with polydopamine, with stiffness value of 1, 10, 30, and 250 kPa, respectively. While the cell spreading increased and the apoptosis decreased with the matrix stiffness, such modulating effect of matrix on cell spreading exhibited different time evolvement behaviors as a function of stiffness, which likely led to surprisingly similar apoptosis rates for the 30 kPa and 250 kPa samples. Matrix stiffness mediated the spreading and apoptosis of MG-63 cells by regulating cell adhesion to matrix and in particular cytoskeletal organization, which was dependent on Ras, Rap1 and PI3K-Akt signaling pathways and finally led to the apoptosis of cancer cells dominated by endoplasmic reticulum stress pathway. Our results provided an insight into the regulation of tumor cell fate by the mechanical clues of ECM, which would have implication for future cancer research and the design of novel anticancer materials.
PubDate: 2023-10-03
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- Pyroptosis Inhibition in Disease Treatment: Opportunities and Challenges
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Abstract: Programmed cell death (PCD) is at the center of immune responses, with different types of PCD occurring based on bodily conditions at a given moment. The main three types of PCD include pyroptosis, necroptosis, and apoptosis. Both pyroptosis and necroptosis induce an inflammatory response while apoptosis avoids eliciting an inflammatory reaction. Recently, pyroptosis has come to the forefront of immunology research due to tremendous potential that has been revealed surrounding the regulators of pyroptosis. In addition to previously known regulators of pyroptosis (ZBP1 and NLRP3 genes), a family of proteins called Gasdermin has been discovered. Specifically, Gasdermin D (GSDMD), when cleaved, participates in the onset of pyroptosis of inflammatory diseases. The N-terminal cleaved portion of the molecule causes cellular membrane openings releasing interleukin-18 and IL-1β, inducing pyroptosis. It is hypothesized that the inhibition of GSDMD using drugs such as Dimethyl Fumarate (DMF) and Disulfiram may halt the progression of certain inflammatory diseases including Multiple Sclerosis (MS), autoimmune encephalitis etc. While there is not yet a concrete treatment for pyroptic cell death in inflammatory disease using GSDMD inhibition, there is ample evidence to suggest that there may be success in future studies and therapeutic applications of GSDMD.
PubDate: 2023-10-02
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- Progress in Understanding the Role and Therapeutic Targets of Polarized
Subtypes of Macrophages in Pulmonary Fibrosis-
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Abstract: Pulmonary fibrosis represents the advanced phase of diverse pulmonary ailments, and at present, a definitive cure for these ailments is lacking. Furthermore, underlying mechanisms causative of these ailments remain elusive. Macrophages are immune cells that resist external stimuli in the early stages after birth. These cells can polarize into the classically (M1) and alternatively (M2) activated macrophages. When stimulated owing to the presence of toxic factors, M1 macrophages produce several pro-inflammatory factors, which mediate the inflammatory injury response of the alveolar tissue. The secretion of diverse growth factors by M2 macrophages contributes to the pathogenesis of aberrant alveolar structural fibrosis and remodeling. The abnormal activity of M2 macrophages is considered a critical factor in the formation of pulmonary fibrosis. In this mini-review, to highlight the clinical implications of research studies, we summarize the role and therapeutic targets of polarized subtypes of macrophages in pulmonary fibrosis and the role of targeting macrophages for the treatment of pulmonary fibrosis.
PubDate: 2023-09-26
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- Activation of Wnt Pathway Suppresses Growth of MUG-Chor1 Chordoma Cell
Line-
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Abstract: Chordoma as a malignant bone tumor, occurs along the axial skeleton and does not have an effective therapy. Brachyury, which is a crucial player for the formation of early embryonic notochord, is abundantly found in both sporadic and familial chordoma. During embryonic development, Brachyury expression was reported to be regulated by the Wnt pathway. The objective of the study is to investigate the role of Wnt signaling in a human chordoma cell line in terms of proliferation, survival, and invasiveness. We tried to elucidate the signaling events that regulate Chordoma cancer. In this regard, Wnt pathway was activated or inhibited using various strategies including small molecules, siRNA-based knockdown and overexpression applications. The results indicated the negative regulatory effect of Wnt signaling activity on proliferation and migration capacity of the chordoma cells. It was revealed that when GSK3β was inhibited, the Wnt pathway was activated and negatively regulated T/Bra expression. Activity of the Wnt pathway caused cell cycle arrest, reduced migration potential of the cells, and led to cell death. Therefore, the present study suggests that the Wnt pathway plays a key role in suppressing the proliferation and invasive characteristics of human chordoma cells and has a great potential as a therapeutic target in further clinical studies.
PubDate: 2023-09-26
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- Impact of Interdependent Ca2+ and IP3 Dynamics On ATP Regulation in A
Fibroblast Model-
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Abstract: The vital participation of Ca2+ in human organ functions such as muscular contractions, heartbeat, brain functionality, skeletal activity, etc, motivated the scientists to thoroughly research the mechanisms of calcium (Ca2+) signalling in distinct human cells. Ca2+, inositol triphosphate (IP3), and adenosine triphosphate (ATP) play important roles in cell signaling and physiological processes. ATP and its derivatives are hypothesized to be important in the pathogenic process that leads to fibrotic illnesses like fibrosis. Fluctuations in Ca2+ and IP3 in a fibroblast cell influence ATP production. To date, no evidence of coupled Ca2+ and IP3 mechanics regulating ATP generation in a fibroblast cell during fibrotic disease has been found. The current work suggests an integrated mechanism for Ca2+ and IP3 dynamics in a fibroblast cell that regulates ATP generation. Simulation has been carried out using the finite element approach. The mechanics of interdependent systems findings vary dramatically from the results of basic independent system mechanics and give fresh information about the two systems’ activities. The numerical results provide new insights into the impacts of disturbances in source influx, the serca pump, and buffers on interdependent Ca2+ and IP3 dynamics and ATP synthesis in a fibroblast cell. According to the findings of this study, fibrotic disorders cannot be attributed solely to disruptions in the processes of calcium signaling mechanics but also to disruptions in IP3 regulation mechanisms affecting the regulation of calcium in the fibroblast cell and ATP release.
PubDate: 2023-09-25
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- SIRT3 Regulates the ROS-FPR1/HIF-1α Axis under Hypoxic Conditions to
Influence Lung Cancer Progression-
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Abstract: Hypoxia-inducible factor (HIF-1α) is a therapeutic target in lung cancer, and the deacetylase sirtuin 3 (SIRT3) is closely associated with tumorigenesis. Formyl peptide receptor 1 (FPR1) is involved in a wide range of physiopathological processes in various tumor cells. We explored whether SIRT3 affects the development of lung cancer by regulating the reactive oxygen species (ROS)-FPR1/HIF-1α axis under hypoxic conditions. The effects of SIRT3 overexpression on the levels of FPR1, HIF-1α, ROS, inflammatory factors, and cell proliferation and migration in A549 cells under hypoxic conditions were assessed in combination with the FPR1 inhibitor. BALB/c nude mice were subcutaneously injected with cancer cells transfected/untransfected with SIRT3 overexpressing lentiviral vectors. Immunohistochemistry and enzyme-linked immunosorbent assay were performed to detect SIRT3 expression and the expression levels of IL-1β, TNF-α, and IL-6, respectively, in tumor tissues. Cell proliferation, invasion, migration, and IL-1β, TNF-α, IL-6, and ROS levels were significantly higher in the Hypoxia group than in the Control group. Moreover, the mRNA and protein expression levels of SIRT3 were significantly down-regulated, whereas they were significantly up-regulated for FPR1 and HIF-1α. In contrast, SIRT3 overexpression in a hypoxic environment inhibited cell proliferation, invasion, and migration, decreased IL-1β, TNF-α, IL-6, and ROS levels, up-regulated the mRNA and protein expression levels of SIRT3, and down-regulated the mRNA and protein expression levels of FPR1 and HIF-1α. In addition, we found the same results in tumorigenic experiments in nude mice. SIRT3 in hypoxic environments may affect tumor cell proliferation, invasion, migration, and inflammation levels via the ROS-FPR1/HIF-1α axis, thereby inhibiting tumor cell development.
PubDate: 2023-09-25
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- Retraction Note: Differentiation of Mesenchymal Stem Cells into Neural
Stem Cells Using Cerebrospinal Fluid-
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PubDate: 2023-09-22
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- Computer-aided Affinity Enhancement of a Cross-reactive Antibody against
Dengue Virus Envelope Domain III-
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Abstract: The dengue virus (DENV), composed of four distinct but serologically related Flaviviruses, causes the most important emerging viral disease, with nearly 400 million infections yearly. Currently, there are no approved therapies. Although DENV infection induces lifelong immunity against the same serotype, the antibodies raised contribute to severe disease in heterotypic infections. Therefore, understanding the mechanism of DENV neutralization by antibodies is crucial in the design of vaccines against all serotypes. This study reports a comparative structural and energetic analysis of the monoclonal antibody (mAb) 4E11 in complex with its target domain III of the envelope protein for all four DENV serotypes. We use extensive replica molecular dynamics simulations in conjunction with the binding free energy calculations. Further single point and double mutations were designed through computational site-directed mutagenesis and observed that the re-engineered antibody exhibits high affinity to binding and broadly neutralizing activity against serotypes. Our results showed improved binding affinity by the gain of enthalpy, which could be attributed to the stabilization of salt-bridge and hydrogen bond interactions at the antigen-antibody interface. The findings provide valuable results in understanding the structural dynamics and energetic contributions that will be helpful to the design of high-affinity antibodies against dengue infections.
PubDate: 2023-09-21
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