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细胞视黄醇结合蛋白-1在体外和体内均由大鼠动脉平滑肌细胞的不同亚群表达。

Cellular retinol-binding protein-1 is expressed by distinct subsets of rat arterial smooth muscle cells in vitro and in vivo.

作者信息

Neuville P, Geinoz A, Benzonana G, Redard M, Gabbiani F, Ropraz P, Gabbiani G

机构信息

Department of Pathology, University of Geneva CMU, Switzerland.

出版信息

Am J Pathol. 1997 Feb;150(2):509-21.

PMID:9033267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1858290/
Abstract

Previous work (M.-L. Bochaton-Piallat, P. Ropraz, F. Gabbiani, G. Gabbiani, Arterioscler Thromb Vasc Biol 1996, 16:815-820) has shown that a subset of smooth muscle cell (SMC) clones derived from the normal rat aortic media displays an epithelioid phenotype similar to that of the whole SMC population cultured from the intimal thickening 15 days after endothelial injury (IT-15). We show here that the whole IT-15 SMC population and the epithelioid clones, derived either from the normal media or from the IT-15, express cellular retinol-binding protein-1 (CRBP-1), a protein involved in retinoid metabolism. The expression of CRBP-1 is accompanied by the expression of cytokeratin 8. In both whole SMC population cultured from IT-15 and epithelioid clones, retinoic acid modulates the transition from the epithelioid phenotype to the spindle phenotype, typical of whole SMC populations cultured from the rat normal aortic media. Moreover, after endothelial injury in vivo, a CRBP-1 expressing SMC subset appears transiently in the IT and disappears, allegedly by apoptosis, when re-endothelialization takes place. Our results suggest that the expression of CRBP-1 is a marker of arterial SMC activation after endothelial injury in vivo and that CRBP-1 and probably retinoids participate in this process.

摘要

先前的研究(M.-L. 博沙顿 - 皮亚拉特、P. 罗普拉兹、F. 加比亚尼、G. 加比亚尼,《动脉硬化、血栓形成和血管生物学》1996年,第16卷:815 - 820页)表明,从正常大鼠主动脉中膜衍生的平滑肌细胞(SMC)克隆的一个亚群表现出与内皮损伤后15天从内膜增厚处(IT - 15)培养的整个SMC群体相似的上皮样表型。我们在此表明,整个IT - 15 SMC群体以及源自正常中膜或IT - 15的上皮样克隆均表达细胞视黄醇结合蛋白 - 1(CRBP - 1),一种参与类视黄醇代谢的蛋白质。CRBP - 1的表达伴随着细胞角蛋白8的表达。在从IT - 15培养的整个SMC群体和上皮样克隆中,视黄酸调节从上皮样表型向纺锤形表型的转变,纺锤形表型是从大鼠正常主动脉中膜培养的整个SMC群体的典型表型。此外,在体内内皮损伤后,一个表达CRBP - 1的SMC亚群短暂出现在内膜增厚处,并且在重新内皮化发生时据称通过凋亡消失。我们的结果表明,CRBP - 1的表达是体内内皮损伤后动脉SMC活化的标志物,并且CRBP - 与可能的类视黄醇参与了这一过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/aa9381ec743a/amjpathol00026-0131-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/f409b734b76b/amjpathol00026-0126-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/44d974b769c4/amjpathol00026-0127-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/c8f97f48d3db/amjpathol00026-0127-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/78e056960bad/amjpathol00026-0128-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/ba46a941ab3e/amjpathol00026-0129-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/e05bd2b1f8dc/amjpathol00026-0129-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/180adc4be50f/amjpathol00026-0130-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/aa9381ec743a/amjpathol00026-0131-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/f409b734b76b/amjpathol00026-0126-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/44d974b769c4/amjpathol00026-0127-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/c8f97f48d3db/amjpathol00026-0127-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/78e056960bad/amjpathol00026-0128-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/ba46a941ab3e/amjpathol00026-0129-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/e05bd2b1f8dc/amjpathol00026-0129-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/180adc4be50f/amjpathol00026-0130-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/667a/1858290/aa9381ec743a/amjpathol00026-0131-a.jpg

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