Induction and maintenance of increased VEGF protein by chronic motor nerve stimulation in skeletal muscle
Induction and maintenance of increased VEGF protein by chronic motor nerve stimulation in skeletal muscle
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DOI：
10.1152/ajpheart.1998.274.3.h860
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发表时间：
1998-03-01
影响因子：
4.8
通讯作者：
Kraus, WE
中科院分区：
文献类型：
--
作者：
Annex, BH;Torgan, CE;Kraus, WE
血管内皮生长因子(VEGF)在体外可促进内皮细胞增殖，在体内可促进血管生成。糖酵解骨骼肌的毛细血管密度低于氧化肌，但当受到慢性运动神经刺激(CMNS)时，可以增加其毛细血管密度，并转变为更氧化的表型。我们使用Western分析和免疫组织化学技术检测了糖酵解骨骼肌CMNS模型和先天性糖酵解氧化表型肌肉中的血管内皮生长因子蛋白。刺激后3天(n=4)、5天(n=2)、10天(n=3)、21天(n=3)和56天(n=2)的肌肉中，每克总蛋白中的血管内皮生长因子蛋白含量分别是对照组的2.9+/-1.0、3.6+/-1.3、3.1+/-0.5、4.4/-1.6和2.7+/-0.3倍。在向氧化表型转变前(3、5和10天)，血管内皮生长因子蛋白表达增加了3.1+/-0.5倍(P<；0.005)，在向氧化表型转变后(2 1和5 6天)仍保持在3.7+/-1倍(P<；0.0 5)。免疫组织化学显示，血管内皮生长因子主要存在于刺激肌纤维之间的基质中，而在肌细胞中未见表达。此外，与氧化肌肉相比，先天糖酵解中的血管内皮生长因子蛋白水平一直较低。这些发现表明，血管内皮生长因子在哺乳动物骨骼肌血管密度的改变和维持中起作用。
Vascular endothelial growth factor (VEGF) causes endothelial cell proliferation in vitro and angiogenesis in vivo. Glycolytic skeletal muscles have a lower capillary density than oxidative muscles but can increase their capillary density and convert to a more oxidative phenotype when subject to chronic motor nerve stimulation (CMNS). We used Western analysis and immunohistochemical techniques to examine VEGF protein in a rabbit CMNS model of glycolytic skeletal muscle and in muscles with innate glycolytic ver sus oxidative phenotypes. VEGF protein per gram of total protein was increased in stimulated vs. control muscles 2.9 +/- 1.0, 3.6 +/- 1.3, 3.1 +/- 0.5, 4.4 +/- 1.6, and 2.7 +/- 0.3 times after 3 (n = 4), 5 (n = 2), 10 (n = 3), 21 (n = 3), and 56 (n = 2) days, respectively. VEGF protein was increased 3.1 +/- 0.5 times (P < 0.005) before (3, 5, and 10 days) and remained elevated 3.7 +/- 1.0 times (P < 0.05) after (21 and 56 days) the transition to an oxidative phenotype. By immunohistochemistry, VEGF protein was found primarily in the matrix between stimulated muscle fibers but not in the myocytes. In addition, VEGF protein was consistently lower in innate glycolytic compared with oxidative muscles. These findings suggest that VEGF plays a role in the alteration and maintenance of vascular density in mammalian skeletal muscles.