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find Keyword "细胞肥大" 4 results
  • 心肌梗死后残存心肌细胞肥大性改变及其IGF1、IGF1R的表达

    目的 观察心肌梗死后残存心肌细胞肥大性改变及其胰岛素样生长因子-1(IGF-1)、胰岛素样生长因子-1受体(IGF-1R)的表达,探讨梗死心肌心肌细胞肥大的机制。 方法 取急性心肌梗死后2周、4周、8周的梗死心肌,制备单心肌细胞悬液,采用激光共聚焦扫描显微镜(Confocal)检测心肌细胞体积,采用免疫组织化学法检测心肌细胞IGF-1、IGF-1R的表达。 结果 〖HTSS〗急性心肌梗死8周梗死区域心肌细胞体积较正常区域心肌细胞增大(37 563.93±6 176.79 μm3 vs. 28 638.61±6 890.89 μm3, t=4.840,P=0.020),细胞肥大以宽度和厚度为主;梗死区域心肌细胞可见IGF1染色阳性颗粒,IGF-1表达高于正常区域心肌细胞(79.58±4.57 vs. 64.12±3.91,t=27.564,P=0.002);IGF-1R主要分布于心肌细胞膜,梗死区域心肌细胞IGF1R表达高于正常区域心肌细胞(67.02±2.56 vs. 66.73±3.49,t=3.845,P=0.042),其中以急性心肌梗死4周IGF-1R表达最高。 结论 心肌梗死后残存心肌细胞分泌IGF-1和IGF-1R,并可能在促使残存心肌细胞肥大中起了积极作用。

    Release date:2016-08-30 05:59 Export PDF Favorites Scan
  • Preliminary Investigation into the Mechanism of Cardiomyocyte Hypertrophy Induced by Visfatin

    The aim of the current study is to investigate the effect of visfatin on cardiomyocyte hypertrophy. Cultured H9c2 cardiomyocytes were exposed to visfatin at different concentrations for different periods of time, and the markers of cardiomyocyte hypertrophy were detected. Moreover, pravastatin, the inhibitor of endoplasmic reticulum stress (ERS) or thapsigargin, an ERS agonist was used respectively to pre-treat the cells before visfatin stimulation. F-actin staining was performed to measure the cell surface change. The mRNA expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP)and ERS markers including glucose-regulated protein 78(GRP78), C/EPB homologous protein (CHOP) and activating transcription factor 6 (ATF6) were assessed by real time RT-PCR. The change of protein level of GRP78 and CHOP was detected by Western blot. The experimental data demonstrated that exposure to 100 or 150 ng/mL concentrations of visfatin for 24 h, or 100 ng/mL of visfatin for 24 or 48 h, significantly increased the expression of markers for cardiomyocyte hypertrophy. Visfatin stimulation provoked ERS in H9c2 cells. Furthermore, pre-treatment with pravastatin partially inhibited the visfatin-induced mRNA expression of ANP and BNP in H9c2 cells, whereas thapsigargin promoted the visfatin-induced expression of cardiomyocyte hypertrophy markers. The results suggest that visfatin might induce cardiomyocyte hypertrophy via ERS -dependent pathways.

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  • RESEARCH PROGRESS OF PATHOLOGY OF ENDOCHONDRAL OSSIFICATION IN OSTEOARTHRITIS

    ObjectiveTo summarize the research progress of pathological manifestations and mechanism of endochondral ossification in osteoarthritis (OA). MethodsThe literature about endochondral ossification, bone-cartilage remodeling in OA, and joints development was reviewed, analyzed, and summarized. ResultsChondrocyte hypertrophy and apoptosis, vascular invasion, replication of the tidemark, thickening calcified cartilage, and thinning superficial cartilage are the characteristics of cartilage degeneration in OA. Articular cartilage and growth plate are similar in structure, and cartilage degeneration in OA is similar to a process of endochondral ossification of the growth plate. ConclusionLoss of stability characterization from resting metabolic balance to a high conversion state of temporary cartilage in stimulation of abnormal mechanical stresses and cytokines would subsequently contributed to continual calcification and remodeling of articular cartilage, which may be the key link of the initiation and development of OA.

    Release date:2016-12-12 09:20 Export PDF Favorites Scan
  • Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy

    This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). In vitro, norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.

    Release date:2020-06-28 07:05 Export PDF Favorites Scan
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