Ran Chen MD  Tiantian Ge MD  Wanying Jiang MD  Junyu Huo MD  Qing Chang MD  Jie Geng MD  Qijun Shan MD  PhD 《Journal of cellular physiology》2019,234(12):21999-22008

Hypertrophic cardiomyopathy (HCM) is reported to be the most common genetic heart disease. To identify key module and candidate biomarkers correlated with clinical prognosis of patients with HCM, we carried out this study with co-expression analysis. To construct a co-expression network of hub genes correlated with HCM, the Weighted Gene Co-expression Network Analysis (WGCNA) was performed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). The protein-protein interaction network analysis of central genes was performed to recognize the interactions of central genes. Gene set enrichment analyses were carried out to discover the possible mechanisms involved in the pathways promoted by hub genes. To validate the hub genes, quantitative real-time polymerase chain reaction (RT-PCR) was performed. Based on the results of topological overlap measure based clustering, 2,351 differentially expressed genes (DEGs) were identified. Those genes were included in six different modules. Of these modules, the yellow and the blue modules showed a pivotal correlation with HCM. DEGs were enriched in immune system procedure associated GO terms and KEGG pathways. We identified nine hub genes (TYROBP, STAT3, CSF1R, ITGAM, SYK, ITGB2, LILRB2, LYN, and HCK) affected the immune system significantly. Among the genes we validated with RT-PCR, TYROBP, CSF1R, and SYK showed significant increasing expression levels in model HCM rats. In conclusion, we identified two modules and nine hub genes, which were prominently associated with HCM. We found that immune system may play a crucial role in the HCM. Accordingly, those genes and pathways might become therapeutic targets with clinical usefulness in the future.  相似文献   

    

Chun-Hua Xu MD  Yue Liu MM  Li-Min Xiao MD  Li-Ke Chen MM  Su-Yue Zheng MM  Er-Ming Zeng MD  Dong-Hai Li MD  You-Ping Li MD 《Journal of cellular physiology》2019,234(12):22272-22284

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Yaron Ilan MD 《Journal of cellular physiology》2019,234(6):7923-7937

Microtubules (MT) and actin microfilaments are dynamic cytoskeleton components involved in a range of intracellular processes. MTs play a role in cell division, beating of cilia and flagella, and intracellular transport. Over the past decades, much knowledge has been gained regarding MT function and structure, and its role in underlying disease progression. This makes MT potential therapeutic targets for various disorders. Disturbances in MT and their associated proteins are the underlying cause of diseases such as Alzheimer’s disease, cancer, and several genetic diseases. Some of the advances in the field of MT research, as well as the potenti G beta gamma, is needed al uses of MT-targeting agents in various conditions have been reviewed here.  相似文献   

    

Farzaneh Chehelcheraghi PhD  Sufan Chien MD  Mohammad Bayat PhD 《Journal of cellular biochemistry》2019,120(10):17491-17499

Random skin flaps (RSFs) are cutaneous flaps. Despite the negative impact of diabetes mellitus (DM) on RSF viability, they are commonly used in diabetic patients. In this study, we have assessed bone marrow mesenchymal stem cell (BMMSC) treatment on RSF survival, tensiometrical parameters, angiogenesis, and mast cells (MCs) count in an ischemic RSF model in rats with type 1 DM (T1DM). We induced T1DM in 30 Wistar adult male rats. The animals were assigned to three groups of 10 rats per group as follows: group 1 (control); group 2 (placebo), and group 3 (BMMSCs). A 30 × 80 mm RSF was created in each rat. On day 7, we measured the viable portion of each RSF. A sample was taken for histological and immunohistochemistry studies, fibroblasts, MCs, angiogenesis, collagen bundle density, and the presence of vascular endothelial growth factor (VEGF)+ cells. An additional sample was taken to evaluate the flap's incision strength. Treatment with BMMSCs (17.8 ± 0.37) significantly increased RSF survival compared with the control (13.3 ± 0.35) and placebo (16.1 ± 0.27) groups (one-way analysis of variance, P = .000; least significant difference, P = .000, P = .002). There was a significant improvement in angiogenesis, as confirmed by stereologic examination. Assessment of VEGF+ cells showed prominent neovascularization in BMMSC-treated RSFs compared with the control and placebo groups. Subdermal injection of BMMSC significantly increased ischemic RSF survival as a result of stimulated neovascularization in T1DM rats. Treatment of diabetic RSF with BMMSCs showed no beneficial effects in the fibroblast number and biomechanical parameters for the repair of ischemic wounds in the rat model. Treatment with BMMSCs significantly increased collagen bundle density.  相似文献   

    

Mohammad Fereidouni PhD  Fateme Arefe Nami MD  Elham Serki MSc  Majid Arefi PhD 《Journal of cellular biochemistry》2019,120(8):13658-13663

Allergic disorders are among the most common diseases around the world especially in children. Many factors contribute to the pathogenesis of atopic disorders, but early events during the pregnancy are very important. The aim of this study was to evaluate the level of cord blood immunoglobulin E (CB-IgE) and its association with maternal in a group of Iranian newborns. In a cross-sectional study, 163 pregnant women randomly selected and information about pregnancy and atopy were taken by questionnaire. Blood samples of mothers and matched cord blood were collected and total serum IgE levels were measured by enzyme-linked immunosorbent assay (ELISA) method. To rolling out the possibility of contamination with maternal blood, total IgA was checked for all the cord blood samples. Sixteen percent of mothers had the history of atopic diseases and the mean IgE level was significantly higher in an atopic than nonatopic mothers (241 vs 102, P < 0.001). About 73.9% of cord blood samples, had high IgE level (>0.9 IU/mL). The level of cord blood IgE (CB-IgE) was not significantly different in male and female newborns (2.14 vs 2.15 IU/mL). There was no significant correlation between maternal factors such as age, pregnancy variables, allergens exposure, smoking, and maternal IgE with cord blood IgE. The results of this study showed that CB-IgE is high in a remarkable number of samples; independent of maternal or fetal factors. Further studies need to evaluate the reasons for the high level of IgE in cord blood in our area.  相似文献   

    

Dong Yin BA  Yongxin Yan BA  Ning Xu BA  Yuan Hui MM  Guanjun Han MM  Ning Ma MM  Chuanhui Yang MM  Guofeng Wang MD 《Journal of cellular biochemistry》2019,120(5):7276-7285

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Amrita Ahluwalia PhD  Michael K. Jones PhD  Neil Hoa MS  Andrzej S. Tarnawski MD  PhD 《Journal of cellular biochemistry》2019,120(7):11651-11659

Gastric epithelial cells are important components of mucosal protection and targets of nonsteroidal anti-inflammatory drugs (NSAIDs)-induced injury. Diclofenac (DFN) is one of the most widely used NSAIDs; however, even its short-term use can induce gastric erosions and ulcers. Nerve growth factor (NGF) has been reported to act not only on neuronal cells but also on endothelial cells; however, its action on gastric epithelial cells is unknown. This study was aimed to determine, whether NGF can protect gastric epithelial cells against DFN-induced injury, and to determine the underlying molecular mechanisms with a focus on mitochondria, survivin, and insulin-like growth factor 1 (IGF-1). Cultured normal rat gastric mucosal epithelial cells 1 (RGM1) were treated with phosphate-buffered saline (PBS; control), NGF (100 ng/mL) and/or DFN (0.25-1.00 mM) for 4 hours. We examined: (1) cell injury by confocal microscopy; (2) cell death/survival using Calcein AM live cell tracking dye; (3) mitochondrial structure and membrane potential function using MitoTracker in live cells; and (4) expression of NGF, its receptor - tropomyosin receptor kinase A (TrkA), survivin and IGF-1 by immunostaining. DFN treatment of RGM1 cells for 4 hours caused extensive cell injury, mitochondrial disintegration, reduced cell viability (from 94 ± 3% in controls to 14 ± 4% in 0.5 mM DFN-treated cells; P < 0.001), and expression of survivin and IGF-1. NGF treatment significantly increased survivin and IGF-1 expression by 41% and 75%, respectively versus PBS controls. Pretreatment with NGF before DFN treatment reduced mitochondrial damage and cell death by 73% and 82%, respectively versus treatment with DFN alone (all P < 0.001). This study also showed the presence of high-affinity TrkA receptors in the plasma membrane and mitochondria of RGM1 cells indicating novel actions of NGF.  相似文献   

    

Qingqing Dai MD  Shujuan Li MD  Ting Liu MD  Jiayin Zheng MD  Song Han MD  Aijuan Qu PhD  Junfa Li MD  PhD 《Journal of cellular biochemistry》2019,120(7):11498-11509

We previously reported that astrocytes are the main sources of interleukin (IL)-17A production that could aggravate neuronal injuries in ischemic stroke. However, the effects of IL-17A on ischemic astrocytes themselves and the underlying molecular mechanism are still unclear. In this study, we found that recombinant mouse (rm) IL-17A could significantly (P < 0.05 or <0.001) alleviate 1-hour oxygen-glucose deprivation (OGD)/reoxygenation (R) 24-hour–induced ischemic injuries in cortical astrocytes with a dose-dependent manner (n = 6 per group). The Western blot and cell cycle analysis results revealed that rmIL-17A significantly ( P < 0.05) inhibited procaspase-3 cleavage without affecting cell proliferation in 1-hour OGD/R 24-hour–treated cortical astrocytes (n = 6 per group). Among the five IL-17 receptor subunits (IL-RA, -RB, -RC, -RD, and -RE), only IL-17RA ( P < 0.01) and -17RC ( P < 0.05) membrane translocation (not messenger RNA and protein) levels were downregulated in cortical astrocytes following 1-hour OGD/reperfusion 24 hours, and rmIL-17A could significantly ( P < 0.05 or <0.001) inhibit this downregulation (n = 6 per group). To further verify the impact of IL-17A on the neurological outcome of ischemic stroke, we found that the intracerebroventricular injection of IL-17A neutralizing monoclonal antibody remarkably ( P < 0.001) reduced the astrocyte activation and improve neurological function ( P < 0.05 or <0.01) of mice following 1-hour middle cerebral artery occlusion/reperfusion (R) 3 to 7 days (n = 6 or 8 per group). These results suggested that IL-17A-mediated alleviation of cortical astrocyte ischemic injuries could affect the neurological outcome of mice with ischemic stroke, which might be mainly dependent on the cell apoptosis pathway through inhibiting the downregulation of IL-17RA and -17RC membrane translocations.  相似文献   

    

Tiago Morais MSc  Barbara Patrício MSc  Sofia Silva Pereira PhD  Sara Andrade PhD  Marcos Carreira PhD  Felipe F. Casanueva MD  PhD  Mariana P. Monteiro MD  PhD 《Journal of cellular biochemistry》2019,120(9):14573-14584

Glucagon-like peptide-1 (GLP-1) influences energy balance by exerting effects on food intake and glucose metabolism, through mechanisms that are partially dependent on the vagal pathway. The aim of this study was to characterize the effects of chronic GLP-1 stimulation on energy homeostasis and glucose metabolism in the absence of vagal innervation Truncal vagotomized (VGX) and sham operated rats (SHAM) received an intraperitoneal GLP-1 infusion (3.5 pmol/kg/min) trough mini-osmotic pumps. To dissect the effects derived from vagal denervation on food intake, an additional group was included consisting of sham operated rats that were PAIR FED to VGX. Food intake and body weight were recorded throughout the experimental period, while the percentage of white and brown adipose tissue, fasting glucose, insulin, gastro-intestinal hormonal profile, hypothalamic, and BAT gene expression were assessed at endpoint. VGX rats had significantly lower food intake, body weight gain, and leptin levels when compared with SHAM rats. Despite having similar body weight, PAIR-FED rats had lower fasting leptin, insulin and insulin resistance, while having higher ghrelin levels than VGX. GLP-1 infusion did not influence food intake or body weight, but was associated with lower leptin levels in VGX and lower pancreatic α-cells ki-67 staining in SHAM. Concluding, this study corroborates that the vagus nerve may modulate whole body energy homeostasis by acting in peripheral signals. Our data suggest that in the absence of vagal or parasympathetic tonus, GLP-1 mediated inhibition of cell proliferation markers in α-cells is prevented, meanwhile leptin suppression, associated with a negative energy balance, is partially overridden.  相似文献   

    

Xiaohui Zhang MM  Renhua Sun MM  Liping Liu MD 《Journal of cellular biochemistry》2019,120(3):4301-4311

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