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首页> 外文期刊>American Journal of Physiology >Extracellular acidosis induces heme oxygenase-1 expression in vascular smooth muscle cells.
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Extracellular acidosis induces heme oxygenase-1 expression in vascular smooth muscle cells.

机译：细胞外酸中毒诱导血管平滑肌细胞中血红素加氧酶-1表达。

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Extracellular acidosis (EA) has profound effects on vascular homeostasis, including vascular bed-specific alterations in vascular tone. Regulation of gene expression by EA has been observed in a variety of cells including vascular endothelial cells. Whether EA regulates gene expression in vascular smooth muscle cells (VSMCs) is not known. Heme oxygenase (HO)-1 is expressed in vascular cells, and its expression is regulated by cellular stressors such as heat, radiation, and hypoxia. Increased HO-1 expression in VSMCs leads to increased production of CO and its second messenger cGMP, which are important regulators of vascular tone and paracrine interactions in the vasculature. We examined whether EA regulates the expression of HO-1 in VSMCs. Exposure of VSMCs to acidic medium (pH 6.8) significantly increased HO-1 mRNA and protein compared with exposure to medium of physiological pH (pH 7.4). The acidic induction of HO-1 expression was time dependent and involved both transcriptional activation of the HO-1 gene and enhanced stability of HO-1 mRNA. Nitric oxide did not appear to mediate this response. We conclude that HO-1 is transcriptionally and posttranscriptionally upregulated by EA in VSMCs. This induction is time dependent and reversible. We speculate that EA, as an important tissue and cellular stressor for VSMCs, may elicit changes in gene expression patterns that contribute to the maintenance or disruption of vascular homeostasis.
机译：细胞外酸中毒（EA）对血管内稳态具有深远的影响，包括血管紧张度的血管床特异性改变。在包括血管内皮细胞的多种细胞中已经观察到EA对基因表达的调节。 EA是否调节血管平滑肌细胞（VSMC）中的基因表达尚不清楚。血红素加氧酶（HO）-1在血管细胞中表达，其表达受诸如热，辐射和缺氧等细胞应激因素的调节。 VSMC中HO-1表达的增加导致CO及其第二信使cGMP的产生增加，这是血管系统中血管张力和旁分泌相互作用的重要调节剂。我们检查了EA是否调节VSMC中HO-1的表达。与暴露于生理pH（pH 7.4）的培养基相比，将VSMC暴露于酸性介质（pH 6.8）会显着增加HO-1 mRNA和蛋白质。 HO-1表达的酸性诱导是时间依赖性的，并且涉及HO-1基因的转录激活和HO-1 mRNA稳定性的增强。一氧化氮似乎没有介导这种反应。我们得出的结论是，HO-1在VSMC中被EA转录和转录后上调。这种感应是时间相关的并且是可逆的。我们推测，EA作为VSMC的重要组织和细胞应激源，可能引起基因表达模式的改变，从而有助于维持或破坏血管稳态。

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