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缺失 cavin 基因揭示了内皮细胞 caveolae 形态发生的组织特异性机制。

Deletion of cavin genes reveals tissue-specific mechanisms for morphogenesis of endothelial caveolae.

机构信息

MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.

出版信息

Nat Commun. 2013;4:1831. doi: 10.1038/ncomms2808.

DOI:10.1038/ncomms2808
PMID:23652019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3674239/
Abstract

Caveolae are abundant in endothelial cells and are thought to have important roles in endothelial cell biology. The cavin proteins are key components of caveolae, and are expressed at varied amounts in different tissues. Here we use knockout mice to determine the roles of cavins 2 and 3 in caveolar morphogenesis in vivo. Deletion of cavin 2 causes loss of endothelial caveolae in lung and adipose tissue, but has no effect on the abundance of endothelial caveolae in heart and other tissues. Changes in the morphology of endothelium in cavin 2 null mice correlate with changes in caveolar abundance. Cavin 3 is not required for making caveolae in the tissues examined. Cavin 2 determines the size of cavin complexes, and acts to shape caveolae. Cavin 1, however, is essential for normal oligomerization of caveolin 1. Our data reveal that endothelial caveolae are heterogeneous, and identify cavin 2 as a determinant of this heterogeneity.

摘要

小窝是内皮细胞中丰富的结构,被认为在内皮细胞生物学中具有重要作用。窖蛋白是小窝的关键组成部分,在不同组织中的表达量不同。在这里,我们使用基因敲除小鼠来确定窖蛋白 2 和 3 在体内小窝形成中的作用。窖蛋白 2 的缺失导致肺和脂肪组织中内皮小窝的丢失,但对心脏和其他组织中内皮小窝的丰度没有影响。窖蛋白 2 缺失小鼠的内皮细胞形态变化与小窝丰度的变化相关。在检查的组织中,窖蛋白 3 不是形成小窝所必需的。窖蛋白 2 决定窖复合物的大小,并作用于小窝的形成。然而,窖蛋白 1 对于窖蛋白 1 的正常寡聚化是必不可少的。我们的数据揭示了内皮小窝是异质的,并确定窖蛋白 2 是这种异质性的决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2e9/3674239/85fb0cded5a2/ncomms2808-f8.jpg
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