...
首页> 外文期刊>Journal of Cellular Physiology >Skeletal muscle cell activation by low-energy laser irradiation: a role for the MAPK/ERK pathway.
【24h】

Skeletal muscle cell activation by low-energy laser irradiation: a role for the MAPK/ERK pathway.

机译:由低能骨骼肌细胞的激活激光辐照:MAPK / ERK的角色途径。

获取原文
获取原文并翻译 | 示例
           

摘要

Low-energy laser irradiation (LELI) has been shown to promote skeletal muscle regeneration in vivo and to activate skeletal muscle satellite cells, enhance their proliferation and inhibit differentiation in vitro. In the present study, LELI, as well as the addition of serum to serum-starved myoblasts, restored their proliferation, whereas myogenic differentiation remained low. LELI induced mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) phosphorylation with no effect on its expression in serum-starved myoblasts. Moreover, a specific MAPK kinase inhibitor (PD098059) inhibited the LELI- and 10% serummediated ERK1/2 activation. However, LELI did not affect Jun N-terminal kinase (JNK) or p38 MAPK phosphorylation or protein expression. Whereas a 3-sec irradiation induced ERK1/2 phosphorylation, a 12-sec irradiation reduced it, again with no effect on JNK or p38. Moreover, LELI had distinct effects on receptor phosphorylation: it caused phosphorylation of the hepatocyte growth factor (HGF) receptor, previously shown to activate the MAPK/ERK pathway, whereas no effect was observed on tumor suppressor necrosis alpha (TNF-alpha) receptor which activates the p38 and JNK pathways. Therefore, by specifically activating MAPK/ERK, but not JNK and p38 MAPK enzymes, probably by specific receptor phosphorylation, LELI induces the activation and proliferation of quiescent satellite cells and delays their differentiation. Copyright 2001 Wiley-Liss, Inc.
机译:低能量激光照射(LELI)已被证明促进骨骼肌再生的体内和激活骨骼肌卫星细胞,增强他们的扩散和抑制在体外分化。LELI以及添加血清serum-starved成肌细胞,恢复了扩散,而肌原性的分化保持在低位。蛋白激酶/细胞外signal-regulated蛋白激酶(MAPK / ERK)磷酸化没有影响其在serum-starved表达式成肌细胞。抑制剂(PD098059)抑制LELI——10%serummediated ERK1/2激活。并不影响小君氨基端激酶(物)或p38MAPK磷酸化或蛋白表达。而一个3秒辐照诱导ERK1/2磷酸化,12秒辐照降低它,再次对物或p38没有影响。对受体LELI有截然不同的影响磷酸化:它的磷酸化作用引起的肝细胞生长因子(HGF)受体,以前MAPK / ERK激活显示途径,而没有观察到肿瘤的影响抑制坏死α(tnf)受体激活p38和物通路。因此,通过具体激活MAPK / ERK,但不是物和p38 MAPK酶可能通过特定的受体磷酸化,LELI诱发静止的激活和增生卫星细胞分化和延迟。版权2001 Wiley-Liss公司。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号