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首页> 外文期刊>Cell and Tissue Research >Cavin-3 (PRKCDBP) deficiency reduces the density of caveolae in smooth muscle
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Cavin-3 (PRKCDBP) deficiency reduces the density of caveolae in smooth muscle

机译：Cavin-3（PRKCDBP）缺乏减少了平滑肌的Caveolae密度

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摘要

Cavins belong to a family of proteins that contribute to the formation of caveolae, which are membrane organelles with functional roles in muscle and fat. Here, we investigate the effect of cavin-3 ablation on vascular and urinary bladder structure and function. Arteries and urinary bladders from mice lacking cavin-3 (knockout: KO) and from controls (wild type: WT) were examined. Our studies revealed that the loss of cavin-3 resulted in similar to 40% reduction of the caveolae protein cavin-1 in vascular and bladder smooth muscle. Electron microscopy demonstrated that the loss of cavin-3 was accompanied by a reduction of caveolae abundance by 40-45% in smooth muscle, whereas the density of caveolae in endothelial cells was unchanged. Vascular contraction in response to an alpha(1)-adrenergic agonist was normal but nitric-oxide-dependent relaxation was enhanced, in parallel with an increased relaxation on direct activation of soluble guanylyl cyclase (sGC). This was associated with an elevated expression of sGC, although blood pressure was similar in WT and KO mice. Contraction of the urinary bladder was not affected by the loss of cavin-3. The proteomic response to outlet obstruction, including STAT3 phosphorylation, the induction of synthetic markers and the repression of contractile markers were identical in WT and KO mice, the only exception being a curtailed induction of the Golgi protein GM130. Loss of cavin-3 thus reduces the number of caveolae in smooth muscle and partly destabilizes cavin-1 but the functional consequences are modest and include an elevated vascular sensitivity to nitric oxide and slightly disturbed Golgi homeostasis in situations of severe cellular stress.
机译：Cavins属于一系列蛋白质，有助于Caveolae的形成，这是肌肉和脂肪中具有功能性作用的膜细胞器。在这里，我们研究了Cavin-3消融对血管和膀胱结构和功能的影响。检查小鼠的动脉和尿膀胱缺乏CAVIN-3（敲除：KO）和来自对照（野生类型：WT）。我们的研究表明，CAVIN-3的损失导致血管和膀胱平滑肌中Caveolae蛋白CAVIN-1减少了40％。电子显微镜证明，Cavin-3的损失伴随着平滑肌的Caveolae丰富的减少40-45％，而内皮细胞中的Caveolae的密度不变。响应α（1） - 肾上腺素能激动剂的血管收缩是正常的，但依赖于氧化物依赖性的弛豫，并平行于可溶性瓜旺环酶（SGC）的直接激活增加。这与SGC的表达升高有关，尽管WT和KO小鼠类似血压。膀胱的收缩不受Cavin-3丧失的影响。对出口梗阻的蛋白质组学反应，包括STAT3磷酸化，合成标记的诱导和收缩标记的抑制在WT和KO小鼠中相同，唯一的例外是GOLGI蛋白GM130的缩减诱导。因此，Cavin-3的丧失减少了平滑肌中的Caveolae的数量，并且部分地稳定的Cavin-1，但功能后果是适度的，并且在严重细胞胁迫的情况下，血管敏感性升高。

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