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Journal Cover Karger Kompass Pneumologie
  [1 followers]  Follow
   Full-text available via subscription Subscription journal
   ISSN (Print) 2296-0368 - ISSN (Online) 2296-0317
   Published by Karger Homepage  [120 journals]
  • Plumbagin Triggers ER Stress-Mediated Apoptosis in Prostate Cancer Cells
           via Induction of ROS
    • Abstract: Background/Aims: Prostate cancer (PCa) is the second most frequently diagnosed cancer in men worldwide. Currently available therapies for hormone-refractory PCa are only marginally effective. Plumbagin (PLB), a natural naphthoquinone isolated from the traditional folk medicine Plumbago zeylanica, is known to selectively kill tumor cells. Nevertheless, antitumor mechanisms initiated by PLB in cancer cells have not been fully defined. Methods: MTT assay was used to evaluate the effect of PLB on the viability of cancer cells. Cell apoptosis and reactive oxygen species (ROS) production were determined by flow cytometry. Protein expression was detected by western blotting. In vivo anti-tumor effect was measured by using tumor xenoqraft model in nude mice. Results: In the present study, we found that PLB decreases cancer cell growth and induces apoptosis in DU145 and PC-3 cells. In addition, by increasing intracellular ROS levels, PLB induced a lethal endoplasmic reticulum stress response in PCa cells. Importantly, blockage of ROS production significantly reversed PLB-induced ER stress activation and cell apoptosis. In vivo, we found that PLB inhibits the growth of PCa xenografts without exhibiting toxicity Treatment of mice bearing human PCa xenografts with PLB was also associated with induction of ER stress activation. Conclusion: Inducing ER stress by PLB thus discloses a previously unrecognized mechanism underlying the biological activity of PLB and provides an in-depth insight into the action of PLB in the treatment of hormone-refractory PCa.
      Cell Physiol Biochem 2018;45:267–280
  • Hypoxia Suppresses TGF-B1-Induced Cardiac Myocyte Myofibroblast
           Transformation by Inhibiting Smad2/3 and Rhoa Signaling Pathways
    • Abstract: Background/Aims: Hypoxia modulation of transforming growth factor (TGF)- β-induced signaling during myofibroblast transformation is dependent on the specific cell type. The purpose of this study was to explore the effects of hypoxia on myofibroblast transformation of TGF-β1-induced cardiomyocyte H9c2 cells. Methods: H9c2 cells were cultured for intermittent hypoxia treatment and TGF-β1 treatment. α-Smooth muscle actin (α-SMA) expression was examined by western blotting and immunofluorescence after treatment. To further explore the possible mechanism for this effect, the effects of hypoxia on three early TGF-β-dependent signaling pathways, i.e. the Smad2/3, RhoA and mitogen-activated protein kinase (MAPK) pathways, were screened by western blotting. Results: Intermittent hypoxia induced TGF-β1 expression, but had no effect on α-SMA expression. Exogenous TGF-β1 alone upregulated α-SMA expression in H9c2 cells in a concentration- and time-dependent manner. α-SMA expression declined with the duration of hypoxia after intermittent hypoxia and exogenous TGF-β1 co-treatment. Phospho-JNK and phospho-p38 levels were not significantly altered after TGF-β1 and hypoxia treatment. However, levels of phospho-ERK increased after TGF-β1 treatment and continued to increase after hypoxia co-treatment. The activation of phospho-Smad2/3 and phospho-RhoA induced by TGFβ1 was significantly reduced after hypoxia co-treatment. Conclusion: Hypoxia can inhibit TGF-β1-induced H9c2 myofibroblast transformation, based on inhibition of α-SMA expression by suppressing signaling downstream of TGF-β1, Smad2/3 and RhoA. It suggested that TGF-β-mediated cardiomyocyte transformation is not involved in hypoxia-mediated fibrosis.
      Cell Physiol Biochem 2018;45:250–257
  • B Subunit of Human Chorionic Gonadotropin Promotes Tumor Invasion and
           Predicts Poor Prognosis of Early-Stage Colorectal Cancer
    • Abstract: Background/Aims: It is well established that many non-trophoblastic tumors secrete HCG (human chorionic gonadotropin) and that such secretion is correlated with the poor prognosis of tumor patients. This study aims to analyze the correlation between β-HCG expression and outcome of colorectal cancer (CRC) and understand its role in CRC pathology Methods: We detected the mRNA and protein expression of β-HCG in human CRC tissues with RT-qPCR and immunohistochemistry, and we compared the clinical-pathological characteristics, prognosis and progression between the β-HCG positive and negative groups. We also generated CRC cell lines with β-HCG over-expression as well as β-HCG stable knockout, and evaluated cell function and mechanism in vitro and in vivo. Results: Fifty out of 136 CRC patients (37%) expressed β-HCG at the invasive front. Clinical-pathological data showed that β-HCG was positively correlated with Dukes staging (P=0.031) and lymph node metastasis (P=0.012). Survival analysis suggested that the patients with high expression of β-HCG had poorer prognosis than those with low β-HCG expression (P=0.0289). β-HCG expression level was also positively correlated with tumor invasion in early-stage CRC patient tissues (P=0.0227). Additionally β-HCG promoted the migration and invasion of CRC in vitro and in vivo but had no effect on the proliferation of tumor cells. Conclusion: Our study demonstrated that β-HCG was ectopically expressed in the CRC patients and its high expression correlated with poor prognosis of early-stage CRC. Additionally it worked as an oncogene that promotes the migration and invasion of CRC by epithelial-mesenchymal transition (EMT).
      Cell Physiol Biochem 2018;45:237–249
  • Circulating MiR-146a May be a Potential Biomarker of Coronary Heart
           Disease in Patients with Subclinical Hypothyroidism
    • Abstract: Background/Aims: Subclinical hypothyroidism (SCH) plays a crucial role in the development and progression of coronary heart disease (CHD). However, any associated changes in the circulating microRNAs (miRNAs) levels and slightly elevated thyroid stimulating hormone (TSH) levels in CHD patients are unknown. miR-146a is a well known miRNA associated with inflammatory autoimmune diseases. Here, we evaluated miR-146a expression in patients, with the goal of re-evaluating the effect of SCH on CHD. Methods: A total of 192 study subjects who underwent coronary angiography for either suspected or confirmed CHD were enrolled in 3 groups: CHD with SCH, CHD alone, and healthy controls. The circulating levels of miR-146a were quantified using qRT-PCR. Results: Levels of miR-146a were positively correlated with CHD severity, as indicated by the Gensini score (r=0.354). The relative expression of miR-146a in the CHD+SCH, CHD and healthy control groups was 2.223±0.827, 1.588±0.726 and 0.632±0.309, respectively. Plasma TSH levels were positively correlated with miR-146a levels (r=0.321). According to multivariate logistic regression analyses, miR-146a levels were associated with the incidence of CHD in patients with SCH. For diagnosing CHD, the area under the ROC curve (AUC) of miR-146a and TSH was 0.779 and 0.752, respectively. When the TSH and miR-146a levels were combined to form a composite panel, the AUC of the panel was 0.858. Conclusion: Plasma miR-146a levels correlated with the severity of coronary atherosclerosis and increased with TSH slightly elevated in patients with CHD. Thus, miR-146a may have good predictive value for CHD among individuals with elevated TSH levels.
      Cell Physiol Biochem 2018;45:226–236
  • Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic
           Seizure via Nrf2/ARE Signaling
    • Abstract: Background/Aims: Ginsenoside Rb1 (Rb1) has been reported to have varieties of neuroprotective effects. This study aimed to evaluate the effects of Rb1 on pentylenetetrazol (PTZ)-induced rat brain injury and Mg2+ free-induced neuron injury and analyzed the detailed molecular mechanisms in vivo and in vitro. Methods: Seizure duration and latency were measured in epilepsy kindled rat. The cognitive impairment was assessed by Morris water maze (MWM) test. Oxidative stress parameters, malondialdehyde (MDA) and glutathione (GSH) were measured by the 2-thiobarbituric acid methods and the DTNB-GSSG reductase recycling methods. Neuronal damage was assessed by hematoxylin and eosin (H#38;E) and Nissl staining. Neuronal apoptosis was measured by Annexin V-FITC and propidium iodide (PI) staining. Immunohistochemistry and immunofluorescence staining were performed to evaluate Nrf2 and HO-1 expressions. Expression of Nrf2, HO-1, Bcl-2, iNOS and LC3 were evaluated by western blot. Results: The PTZ-injured rats presented longer seizure duration and shorter seizure latency. Rb1 ameliorated these effects, as well as the cognitive deficits caused by PTZ exposure. Besides, Rb1 dose-dependently increased GSH levels, decreased MDA levels and alleviated neuronal damage in PTZ-treated rats. In vitro, Rb1 increased cell viability and decreased neuronal apoptosis in a dose-dependent manner under Mg2+ free condition. Moreover, in vivo and in vitro, Rb1 enhanced both the Nrf2 and HO-1 expressions. Furthermore, upregulation of the expression of Bcl-2 and downregulation of the expression of iNOS and LC3 were observed. However, knockdown of Nrf2 adversely affected the protective effects of Rb1 in epileptic hippocampal neurons. Conclusion: Rb1 conferred neuroprotective effects against PTZ-induced brain damage and Mg2+ free-induced neuron injury by activating Nrf2/ARE signaling.
      Cell Physiol Biochem 2018;45:212–225
  • Molecular Genetic Mechanisms of Hereditary Spherocytosis: Current
    • Abstract: With the widespread use of genetic diagnostic technologies, many novel mutations have been identified in hereditary spherocytosis (HS)-related genes, including SPTA1, SPTB, ANK1, SLC4A1, and EPB42. However, mutations in HS-related genes are dispersed and nonspecific in the diagnosis of some HS patients, indicating significant heterogeneity in the molecular deficiency of HS. It is necessary to provide the molecular and genetic characteristics of these 5 genes for clinicians to examine HS. Here, we reviewed the recent proposed molecular genetic mechanisms of HS.
      Acta Haematol 2018;139:60–66
  • Statins and New-Onset Diabetes in Cardiovascular and Kidney Disease
           Cohorts: A Meta-Analysis
    • Abstract: Background: Statins have long been prescribed for the primary and secondary prevention of cardiovascular disease (CVD) and kidney disease. Their benefits and efficacy are widely accepted in current clinical practice, but like any other therapeutic agents, they have adverse effects. One of the emerging concerns with statin therapy is the development of new-onset diabetes mellitus (NODM), a dreaded risk factor for CVD and kidney disease and widely viewed as CVD equivalent. Accumulating evidence indicates that NODM is a consequence of statin use. Methods: We conducted a meta-analysis of studies reporting on associations between NODM and statin use. Based on strict exclusion criteria, a total of 11 studies were selected. Their data were analyzed using Comprehensive Meta-Analysis® statistical software and reported as odds ratios (OR) with 95% confidence intervals (CI). Results: The cumulative fixed effect for use of statin therapy and incident NODM was an OR of 1.61 (95% CI 1.55–1.68, p #x3c; 0.001). Our results suggest that statin therapy is associated with NODM, such that there is a small but significant risk of NODM among patients receiving statin for CVD prevention therapy. However, this high-risk population also has other diabetes risk factors (such as obesity and hypertension) contributing to the development of NODM. Conclusions: It is imperative that patients on statin therapy be monitored carefully for NODM. However, it can be argued that the risk of statin therapy is offset by the multitude of cardiovascular and kidney-protective effects provided by such an important and highly effective therapeutic agent.
      Cardiorenal Med 2018;8:105–112
  • The Role of Dendritic and Endothelial Cells in Cardiorenal Syndrome
    • Abstract: Backgrounds: Dendritic cells (DCs) are antigen-presenting cells that play a central role in innate and adaptive immune responses; however, the cross talk between cardiac and renal DCs in cardiorenal syndrome (CRS) has not yet been fully elucidated. In this setting, endothelial cells (ECs) also contribute to immune responses. Summary: DC and EC activation and dysfunction have a central role in the pathogenesis of CRS. Regarding immune responses in CRS, it is unknown whether ECs may serve as antigen-presenting cells or act synergistically with DCs to actively participate in innate and adaptive immune responses. This review first focuses on the burden of concomitant heart and renal DCs in the context of CRS; it examines what is known of DCs in animal models, and proposes a central role for DCs in all types of CRS. Second, this review briefly describes the role of ECs in the context of CRS. Key Messages: Understanding the role of DCs and ECs in immune response could lead to the development of novel therapies for the prevention and treatment of CRS.
      Cardiorenal Med 2018;8:92–104
  • Clinical Characteristics and Allergen Sensitization Patterns of Patients
           with Local Allergic Rhinitis in Southern China
    • Abstract: Background: Local allergic rhinitis (LAR) is characterized by the production of specific IgE (sIgE) in the nasal mucosa without evidence of systemic atopy. The characteristics of LAR in Caucasians have been well documented. LAR is understudied in China, with prevalence, patient demographics, symptomatology, and the allergen sensitization profile being poorly understood. The purpose of this study is to investigate the demographics, characteristics, and allergen sensitization profile of patients with LAR in Southern China. Methods: A total of 194 patients with rhinitis and 13 healthy subjects were enrolled in the current study. The patients' demographic data, clinical history, and symptoms were recorded. Local and systemic sIgE to a wide panel of specific allergens were measured in the nasal secretion and serum samples. Results: Among the rhinitis patients, 115 were classified as allergic rhinitis (AR; 59.3%), 15 as LAR (7.7%), and 64 as non-AR (33.0%). The demographic characteristics, duration, frequency, and severity of symptoms were similar, although LAR exhibited higher symptom scores for nasal itch. Monosensitization was the predominant pattern of sensitization in both AR (109 out of 115, 95%) and LAR (14 out of 15, 93%). House dust mite was the dominant allergen in AR patients (109 out of 115, 95%), while pollen was the dominant allergen in LAR patients (11 out of 15, 73%). Conclusion: The prevalence of LAR patients in Southern China was 7.7%. Pollen was the most common sensitizing allergen for the local LAR patients, which differs from Caucasian studies, in which house dust mite was the dominant sensitizing allergen. Monosensitization was the predominant pattern in both AR and LAR.
      Int Arch Allergy Immunol
  • Call for Nomination of Members of the International Standing Committee of
           Human Cytogenomic Nomenclature
    • Abstract:
      Cytogenet Genome Res 2017;153:55
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
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Fax: +00 44 (0)131 4513327
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