Skeletal muscle-endothelial cell cross talk through angiotensin II
Skeletal muscle-endothelial cell cross talk through angiotensin II
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DOI：
10.1152/ajpcell.00306.2010
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发表时间：
2010-12-01
影响因子：
5.5
通讯作者：
Parise, Gianni
中科院分区：
文献类型：
--
作者：
Bellamy, Leeann M.;Johnston, Adam P. W.;Parise, Gianni
张建军，张建军，张建军。血管紧张素对骨骼肌内皮细胞串扰的影响。[J] .中国生物医学工程学报，2016,31(2):387 - 398。首次发表于2010年9月22日；doi: 10.1152 / ajpcell.00306.2010。血管紧张素II （ANG II）在出生后血管生成和骨骼肌（SKM）再生过程中的血管生成中的作用尚不清楚。我们检测了ACE抑制剂处理的angii型1a受体敲除（AT1a(-/-)）和C57Bl/6对照小鼠在心脏毒素诱导的肌肉再生过程中，ANG II刺激毛细血管形成和生长的能力。胫骨前肌（TA）横断面分析显示，与对照组相比，损伤后21天，AT1a（-/-）和卡托普利治疗小鼠的毛细血管化分别减少了17%和23%。相反，在早期时间点（7天和10天）没有检测到毛细血管化的差异。这些结果表明ANG II是血管生成的调节剂，而不是体内血管生成的调节剂。人脐静脉内皮细胞（HUVECs）体外血管生成实验进一步证实了ANG II的促血管生成作用，ANG II处理后，血管长度和分支点数量分别增加71%和124%。重要的是，用分化肌肉细胞的条件培养基处理HUVECs，与对照组相比，管长和分支点数增加了84%和203%，在用血管紧张素转换酶抑制剂预处理细胞后，这一现象被消除了。ANG II的促血管生成作用可归因于内皮细胞迁移的增强，因为transwell和琼脂糖迁移试验分别显示细胞运动性增加37%和101%。总的来说，这些数据突出了ANG II在体内SKM再生过程中的促血管生成调节剂作用，更重要的是表明SKM释放的ANG II可以向内皮细胞发出信号，并通过诱导内皮细胞迁移来调节血管生成。
Bellamy LM, Johnston AP, De Lisio M, Parise G. Skeletal muscle-endothelial cell cross talk through angiotensin II. Am J Physiol Cell Physiol 299: C1402-C1408, 2010. First published September 22, 2010; doi:10.1152/ajpcell.00306.2010.-The role of angiotensin II (ANG II) in postnatal vasculogenesis and angiogenesis during skeletal muscle (SKM) regeneration is unknown. We examined the capacity of ANG II to stimulate capillary formation and growth during cardiotoxin-induced muscle regeneration in ACE inhibitor-treated ANG II type 1a receptor knockout (AT1a(-/-)) and C57Bl/6 control mice. Analysis of tibialis anterior (TA) cross-sections revealed 17% and 23% reductions in capillarization in AT1a(-/-) and captopril treated mice, respectively, when compared with controls, 21 days postinjury. Conversely, no differences in capillarization were detected at early time points (7 and 10 days). These results identify ANG II as a regulator of angiogenesis but not vasculogenesis in vivo. In vitro angiogenesis assays of human umbilical vein endothelial cells (HUVECs) further confirmed ANG II as proangiogeneic as 71% and 124% increases in tube length and branch point number were observed following ANG II treatment. Importantly, treatment of HUVECs with conditioned media from differentiated muscle cells resulted in an 84% and 203% increase in tube length and branch point number compared with controls, which was abolished following pretreatment of the cells with an angiotensin-converting enzyme inhibitor. The pro-angiogenic effect of ANG II can be attributed to an enhanced endothelial cell migration because both transwell and under agarose migration assays revealed a 37% and 101% increase in cell motility, respectively. Collectively, these data highlight ANG II as a proangiogenic regulator during SKM regeneration in vivo and more importantly demonstrates that ANG II released from SKM can signal endothelial cells and regulate angiogenesis through the induction of endothelial cell migration.