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.
中科院分区:
文献类型:
--
作者:
Smith, Cheryl A.;Stauber, Franciose;Stauber, William T.
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.