Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis
Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis
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DOI：
10.1152/ajpregu.00347.2010
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发表时间：
2010-10-01
影响因子：
2.8
通讯作者：
Breen, Ellen C.
中科院分区：
文献类型：
--
作者：
Olfert, I. Mark;Howlett, Richard A.;Breen, Ellen C.
Olfert IM, Howlett RA, Wagner PD, Breen EC。肌细胞血管内皮生长因子是运动诱导的骨骼肌血管生成所必需的。[J] .中国生物医学工程学报，2016,33(2):559 - 567。首次发表于2010年8月4日；doi: 10.1152 / ajpregu.00347.2010。我们之前使用Cre-LoxP策略表明，血管内皮生长因子（VEGF）对于久坐成年小鼠骨骼肌毛细血管的发育和维持是必需的。为了确定骨骼肌毛细血管适应运动训练是否需要VEGF的表达，我们以相同的跑步速度在跑步机上跑步6周（1小时/天，5天/周）后，测量了肌细胞特异性VEGF基因缺失（mVEGF(-/-)）和野生型（WT）窝代小鼠腓肠肌毛细血管。在mVEGF（-/-）和WT小鼠中，还评估了训练对代谢酶活性水平和全身跑步性能的影响。WT小鼠训练后腓肠肌深层肌区毛细血管密度显著增加59% (P < 0.05)，而mVEGF（-/-）小鼠训练后毛细血管密度无明显变化。训练后，WT小鼠的最大跑步速度和亚最大跑步时间分别增加了20%和13% (P < 0.05)，而mVEGF（-/-）小鼠的最大跑步速度和亚最大跑步时间不变。训练导致WT和mVEGF（-/-）小鼠骨骼肌柠檬酸合成酶（CS）和磷酸果糖激酶（PFK）活性增加（P < 0.05），而β -羟酰基辅酶a脱氢酶（β - had）活性仅在WT小鼠中增加。这些数据表明，在没有肌细胞表达VEGF的情况下，骨骼肌毛细血管对体育训练的适应不会发生。然而，骨骼肌对运动训练的代谢适应是独立于肌细胞VEGF表达的。
Olfert IM, Howlett RA, Wagner PD, Breen EC. Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis. Am J Physiol Regul Integr Comp Physiol 299: R1059-R1067, 2010. First published August 4, 2010; doi:10.1152/ajpregu.00347.2010.-We have previously shown, using a Cre-LoxP strategy, that vascular endothelial growth factor (VEGF) is required for the development and maintenance of skeletal muscle capillarity in sedentary adult mice. To determine whether VEGF expression is required for skeletal muscle capillary adaptation to exercise training, gastrocnemius muscle capillarity was measured in myocyte-specific VEGF gene-deleted (mVEGF(-/-)) and wild-type (WT) littermate mice following 6 wk of treadmill running (1 h/day, 5 days/wk) at the same running speed. The effect of training on metabolic enzyme activity levels and whole body running performance was also evaluated in mVEGF(-/-) and WT mice. Posttraining capillary density was significantly increased by 59% (P < 0.05) in the deep muscle region of the gastrocnemius in WT mice but did not change in mVEGF(-/-) mice. Maximal running speed and time to exhaustion during submaximal running increased by 20 and 13% (P < 0.05), respectively, in WT mice after training but were unchanged in mVEGF(-/-) mice. Training led to increases in skeletal muscle citrate synthase (CS) and phosphofructokinase (PFK) activities in both WT and mVEGF(-/-) mice (P < 0.05), whereas beta-hydroxyacyl-CoA dehydrogenase (beta-HAD) activity was increased only in WT mice. These data demonstrate that skeletal muscle capillary adaptation to physical training does not occur in the absence of myocyte-expressed VEGF. However, skeletal muscle metabolic adaptation to exercise training takes place independent of myocyte VEGF expression.