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首页> 外文期刊>American Journal of Physiology >Involvement of transforming growth factor-beta in regulation of calcium transients in diabetic vascular smooth muscle cells.
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Involvement of transforming growth factor-beta in regulation of calcium transients in diabetic vascular smooth muscle cells.

机译：转化生长因子-β参与糖尿病血管平滑肌细胞钙瞬变的调节。

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摘要

Altered calcium [Ca2+] transients of vascular smooth muscle cells to vasoconstrictors may contribute to altered regulation of blood flow in diabetes. We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels. Aortic vascular smooth muscle cells isolated from diabetic rats exhibited markedly impaired ANG II-induced cytosolic calcium [Ca2+] signal that was completely restored by pretreatment with anti-TGF-beta antibodies. Similar findings were noted in microvascular smooth muscle cells isolated from preglomerular vessels and cultured in high glucose. The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2. In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta. The characteristic increase in glomerular filtration surface area found in diabetic rats was prevented by treatment with anti-TGF-beta antibodies, and impaired ANG II-induced aortic ring contraction in diabetic rats was completely restored by anti-TGF-beta antibodies. Impaired vascular dysfunction may be partly due to decreased inositol 1,4,5-trisphosphate receptor (IP3R), as reduced type I IP3R expression was found in diabetic aorta and restored by anti-TGF-beta antibodies. We conclude that TGF-beta plays an important role in the vascular dysfunction of early diabetes by inhibiting calcium transients in vascular smooth muscle cells.
机译：血管平滑肌细胞向血管收缩剂的钙[Ca2 +]瞬变改变可能有助于糖尿病患者血流调节的改变。我们推测糖尿病诱导的转化生长因子（TGF）-β产生有助于大血管和微血管中血管平滑肌细胞的ANG II反应受损。从糖尿病大鼠中分离出的主动脉血管平滑肌细胞显示出明显受损的ANG II诱导的胞质钙[Ca2 +]信号，该信号可通过用抗TGF-β抗体进行预处理而完全恢复。从肾小球前血管分离并在高葡萄糖中培养的微血管平滑肌细胞中也发现了类似的发现。通过向培养的主动脉平滑肌细胞中添加TGF-beta1和-beta2亚型，可以复制糖尿病对[Ca2 +]瞬变的影响，并且糖尿病细胞具有提高的TGF-beta2产量。在体内条件下，糖尿病肾小球中TGF-β1增加，而糖尿病主动脉中TGF-β2增加。抗TGF-β抗体可预防糖尿病大鼠肾小球滤过表面积的特征性增加，抗TGF-β抗体可完全恢复受损的ANG II诱导的糖尿病大鼠主动脉环收缩。血管功能障碍受损可能部分归因于肌醇1,4,5-三磷酸受体（IP3R）降低，因为在糖尿病主动脉中发现I型IP3R表达降低，并被抗TGF-β抗体恢复。我们得出的结论是，TGF-β通过抑制血管平滑肌细胞中的钙瞬变，在早期糖尿病的血管功能障碍中起重要作用。

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