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首页> 外文期刊>American Journal of Physiology >Role of smooth muscle protein SM22alpha in glomerular epithelial cell injury
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Role of smooth muscle protein SM22alpha in glomerular epithelial cell injury

机译：平滑肌蛋白SM22α在肾小球上皮细胞损伤中的作用

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Podocytes are considered terminally differentiated cells in the mature kidney under normal conditions. In the face of injury, podocytes may proceed along several possible pathways, including dedifferentiation and proliferation, persistent cell cycle arrest, hypertrophy, apoptosis, or necrosis. There is mounting evidence that transdifferentiation into a dysregu-lated phenotype may also be a potential cell fate. We have previously reported that the transcript of SM22alpha, an actin-binding protein considered one of the earliest markers of smooth muscle differentiation, is upregulated nearly 70-fold in glomeruli of rats with passive Hey-mann nephritis (PHN). In contrast, the SM22alpha transcript is absent in normal adult rat glomeruli. The purpose of this study was to define SM22a's expression during kidney development and its role in glomerular diseases characterized by podocyte injury and proteinuria. During glomerulogenesis and podocyte differentiation, SM22alpha was expressed in glomeruli. This expression disappeared with glomerular maturation. Along with SM22alpha induction in PHN, confirmed at both mRNA and protein levels, SM22a was also induced across a broad range of proteinuric diseases, including experimental animal models (puromycin aminonucleoside nephropathy, adriamycin nephropathy, passive nephrotoxic nephritis, and diet-induced obesity) and human diseases (collapsing glomerulopathy, diabetic nephropathy, classic focal segmental glomerulosclerosis, IgA nephropathy, minimal-change disease, membranous nephropathy, and membranoprolifera-tive glomerulonephritis). Crescentic glomerulonephritis was induced in SM22alpha +/+ and SM22alpha -/- mice by intraperitoneal injection of sheep anti-rabbit glomeruli antibody 12.5 mg/20 g body wt X 2 doses in = 12-15/group), with mice euthanized at 7 and 14 days. Compared with SM22alpha -/- mice, SM22alpha +/+ mice demonstrated worse disease by histopathological parameters. In addition, there was greater apoptosis (cleav...
机译：在正常情况下，足细胞被认为是成熟肾脏中的终末分化细胞。面对损伤，足细胞可能会沿着几种可能的途径前进，包括去分化和增殖，持续的细胞周期停滞，肥大，细胞凋亡或坏死。越来越多的证据表明，转分化为功能障碍的表型也可能是潜在的细胞命运。我们以前曾报道过，SM22alpha是肌动蛋白结合蛋白，被认为是平滑肌分化的最早标志之一，其转录本在被动性Hey-mann肾炎（PHN）大鼠肾小球中被上调了近70倍。相反，正常成年大鼠肾小球中不存在SM22alpha转录物。这项研究的目的是定义SM22a在肾脏发育过程中的表达及其在以足细胞损伤和蛋白尿为特征的肾小球疾病中的作用。在肾小球发生和足细胞分化过程中，SM22alpha在肾小球中表达。该表达随着肾小球成熟而消失。除了在mRNA和蛋白质水平均已证实的PHN中的SM22alpha诱导作用之外，SM22a还可以在多种蛋白尿疾病中被诱导，包括实验动物模型（嘌呤霉素氨基核苷肾病，阿霉素肾病，被动性肾毒性肾炎和饮食引起的肥胖）和人类疾病（合并性肾小球病，糖尿病性肾病，经典的局灶性节段性肾小球硬化，IgA肾病，微小变化疾病，膜性肾病和膜增生性肾小球性肾炎）。通过腹膜内注射绵羊抗兔肾小球​​抗体12.5 mg / 20 g体重X 2剂量（= 12-15 /组），在SM22alpha + / +和SM22alpha-/-小鼠中诱发新月型肾小球肾炎，小鼠在7和14天与SM22alpha-/-小鼠相比，SM22alpha + / +小鼠的组织病理学参数显示病情较差。此外，细胞凋亡更大（裂解...

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