Transforming growth factor-β following skeletal muscle strain injury in rats

Transforming growth factor-β following skeletal muscle strain injury in rats
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DOI:
10.1152/japplphysiol.01503.2005
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发表时间:
2007-02-01
影响因子:
3.3
通讯作者:
Stauber, William T.
Stauber, William T.
中科院分区:
医学2区
文献类型:
--
作者:
Smith, Cheryl A.;Stauber, Franciose;Stauber, William T.

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大鼠骨骼肌拉伤后转化生长因子β的变化。J Appl Physiol 102:755-761,2007.首次发表于2006年10月26日; doi:10.1152/japplphysiol.01503.2005。转化生长因子-β(TGF-β)是与炎症过程、伤口愈合和纤维化有关的多功能细胞因子。在肌肉疾病(即,营养不良和炎性肌病)和肌肉损伤的动物模型(即,由于心脏毒素、撕裂和离心性收缩产生),增加的TGF-β与肌肉纤维化和愈合有关。虽然TGF-β转录本丰度在损伤后增加,但许多研究认为TGF-β蛋白也有活性,如胶原蛋白转录本丰度增加所证明的。目的是确定TGF-β蛋白是否存在,并在损伤后48小时起作用。使用雌性大鼠,通过拉伸(50次拉伸)足底屈肌肌肉产生肌肉拉伤。损伤后48小时,取出内侧腓肠肌并将其分成5个相等的节段。用细胞内伴刀豆球蛋白A染色计数受损的肌纤维。损伤的肌纤维的百分比显着更大的最远段。通过免疫组织化学、RT-PCR和免疫印迹分析评估TGF-β。免疫组织化学显示在肌纤维损伤区域存在TGF-β(1),而未检测到TGF-β(2)。通过RT-PCR分析记录了应变损伤后TGF-β(1)和TGF-β(2)转录丰度的增加。通过免疫印迹分析,在应变损伤后观察到TGF-β(1)和TGF-β(2)前体丰度增加,但活性TGF-β丰度没有变化。虽然细胞损伤量与TGF-β转录和蛋白丰度之间没有相关性,但在损伤后48小时,应变损伤的骨骼肌中存在TGF-β(1)和TGF-β(2)前体蛋白水平升高。
Transforming growth factor-beta following skeletal muscle strain injury in rats. J Appl Physiol 102: 755-761, 2007. First published October 26, 2006; doi:10.1152/japplphysiol.01503.2005.-Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine implicated in inflammatory processes, wound healing, and fibrosis. In muscle diseases (i.e., dystrophy and inflammatory myopathy) and in animal models of muscle injury (i.e., produced by cardiotoxin, laceration, and eccentric contractions), increased TGF-beta was associated with muscle fibrosis and healing. Although TGF-beta transcript abundance was increased following injury, many studies presume that TGF-beta protein was also active as evident by increases in collagen transcript abundance. The purpose was to determine whether TGF-beta protein is present and active 48 h following injury. Using female rats, muscle strains were produced by stretching (50 stretches) the plantar flexor muscles. Forty-eight hours following injury, the medial gastrocnemius was removed and compartmentalized into five equal segments. Damaged myofibers with intracellular concanavalin A staining were counted. The percentage of damaged myofibers was significantly greater in the distal-most segment. TGF-beta was assessed by using immunohistochemistry, RT-PCR, and immunoblot analysis. Immunohistochemistry revealed the presence of TGF-beta(1) in areas of myofiber injury, whereas TGF-beta(2) was not detected. Increases in TGF-beta(1) and TGF-beta(2) transcript abundance following strain injury were documented by RT-PCR analysis. Increases in TGF-beta(1) and TGF-beta(2) precursor abundance were observed following strain injury by using immunoblot analysis but there was no change in active TGF-beta abundance. Although there was no correlation between the amount of cellular injury and TGF-beta transcript and protein abundance, elevated levels of TGF-beta(1) and TGF-beta(2) precursor proteins were present in strain-injured skeletal muscles 48 h after injury.