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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >LOX-1 in the maintenance of cytoskeleton and proliferation in senescent cardiac fibroblasts.
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LOX-1 in the maintenance of cytoskeleton and proliferation in senescent cardiac fibroblasts.

机译：LOX-1在衰老的心脏成纤维细胞中维持细胞骨架和增殖。

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摘要

Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) is one of the most important receptors for binding and uptake of ox-LDL in endothelial cells, vascular smooth muscle cells and cardiomyocytes. In this study in cultured mice heart fibroblasts, we describe a decrease in LOX-1 expression as these cells go through successive passages. Further, fibroblast aging is associated with significant changes in morphology and proliferation ability. The same phenomena were observed in primary cardiac fibroblasts isolated from the aged mice (130-week). We also noted that the senescent fibroblasts have increased susceptibility to apoptosis and have a disorganized cytoskeleton. To ascertain the contribution of LOX-1 in the decline in proliferative ability and morphological changes in the aged cells, senescent fibroblasts were transfected with h-LOX-1. Transfection with h-LOX-1 resulted in cytoskeleton reorganization and partial restoration of the expression of related proteins, CDC42 and p70 S6 kinase. Upregulation of LOX-1 also significantly enhanced their proliferation potential and restored the expression of related genes Mdm2 and phos-Akt, and modestly reduced the expression of aging markers 4-HNE and β-catenin. These findings suggest that LOX-1 contributes, at least in part, to the process of fibroblast senescence and may be viewed as a new aging maker.
机译：凝集素样氧化型低密度脂蛋白受体1（LOX-1）是内皮细胞，血管平滑肌细胞和心肌细胞中ox-LDL结合和摄取的最重要的受体之一。在对培养的小鼠心脏成纤维细胞的这项研究中，我们描述了LOX-1表达的降低，因为这些细胞经过连续传代。此外，成纤维细胞老化与形态和增殖能力的显着变化有关。在从老年小鼠中分离的原代心脏成纤维细胞（130周）中观察到了相同的现象。我们还注意到衰老的成纤维细胞对细胞凋亡的敏感性增加，并且细胞骨架紊乱。为了确定LOX-1在衰老细胞的增殖能力下降和形态变化中的作用，用h-LOX-1转染衰老的成纤维细胞。用h-LOX-1转染导致细胞骨架重组和相关蛋白CDC42和p70 S6激酶表达的部分恢复。 LOX-1的上调也显着增强了它们的增殖潜能，并恢复了相关基因Mdm2和phos-Akt的表达，并适度降低了衰老标记物4-HNE和β-catenin的表达。这些发现表明，LOX-1至少部分地促进了成纤维细胞的衰老过程，并可能被视为新的衰老制造者。

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