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通过原位杂交对动脉粥样硬化斑块中基质溶解素基因表达进行定位。

Localization of stromelysin gene expression in atherosclerotic plaques by in situ hybridization.

作者信息

Henney A M, Wakeley P R, Davies M J, Foster K, Hembry R, Murphy G, Humphries S

机构信息

Arterial Diseases Unit, Charing Cross Sunley Research Centre, Hammersmith, London, England.

出版信息

Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8154-8. doi: 10.1073/pnas.88.18.8154.

DOI:10.1073/pnas.88.18.8154
PMID:1896464
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC52465/
Abstract

The stromelysins are members of a family of extracellular matrix metalloproteinases. These enzymes may erode the connective tissue in atherosclerotic plaques, leading to fissuring and acute thrombotic events. Cell-specific stromelysin expression in human atherosclerotic plaques was studied by in situ hybridization and immunocytochemistry. Sections were taken from nine coronary arteries: eight with well-established plaques and one normal. Unambiguous signals were seen in five plaques, two were inconclusive, and the remaining sample was negative, as was the normal coronary artery. Stromelysin mRNA transcripts were localized to isolated individual cells, some of which were smooth muscle, in the plaque cap, intima, and adventitia, but not the media. Expression was also seen in large clusters of macrophages that contained intracellular lipid deposits. The isolated expression of stromelysin by smooth muscle cells may reflect local connective tissue remodeling associated with growth and the formation of the plaque, whereas the more extensive expression associated with macrophages may be of greater pathological significance, contributing to the destabilization of the extracellular matrix and eventual plaque rupture.

摘要

基质溶解素是细胞外基质金属蛋白酶家族的成员。这些酶可能会侵蚀动脉粥样硬化斑块中的结缔组织,导致斑块破裂和急性血栓形成事件。通过原位杂交和免疫细胞化学研究了人类动脉粥样硬化斑块中细胞特异性基质溶解素的表达。从九条冠状动脉取材:八条有成熟斑块,一条正常。在五个斑块中观察到明确的信号,两个不确定,其余样本为阴性,正常冠状动脉也是如此。基质溶解素mRNA转录本定位于斑块帽、内膜和外膜中分离的单个细胞,其中一些是平滑肌细胞,但中膜未见。在含有细胞内脂质沉积的大量巨噬细胞簇中也观察到表达。平滑肌细胞单独表达基质溶解素可能反映了与斑块生长和形成相关的局部结缔组织重塑,而与巨噬细胞相关的更广泛表达可能具有更大的病理意义,导致细胞外基质不稳定并最终导致斑块破裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/1f9276730779/pnas01068-0263-f.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/2fb76840136d/pnas01068-0262-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/316a771e0ded/pnas01068-0262-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/b2a3342864d0/pnas01068-0262-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/96d432fd59b2/pnas01068-0262-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/2ea8b5d2e0ff/pnas01068-0262-f.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/3b91719c850c/pnas01068-0263-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe10/52465/592b76d18f30/pnas01068-0263-c.jpg
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