期刊文献+

急性递增负荷运动对大鼠心肌JAKs及SOCS1表达的影响 被引量:2

Expressions of JAKs and SOCS1 in myocardium induced by acute exercise
下载PDF
导出
摘要 目的测定JAK家族成员以及SOCS1在运动后心肌的表达,以探讨它们在运动心肌JAK/STAT信号通路中可能的相互作用。方法雄性SD大鼠进行递增负荷跑台运动,采用免疫组化法观察运动后0、1、3、5、、12和24h心肌JAK1、JAK3和SOCS1的表达。结果运动后即刻大鼠心肌细胞JAKl的表达显著加强,并持续到运动后24h;而大鼠心肌细胞JAK3及SOCS1的表达在运动后1~5h显著降低,两者在运动后12h恢复到安静水平。结论急性运动中,JAK1和JAK3对运动心脏功能的调节可能作用不同,SOCS1可能参与了运动心肌JAKs/STAT3信号通路的调节过程。 Objective To evaluate Janus kinase(JAK)s and SOCS1 expression in myocardium induced by acute exercise in order to understand the possible regulating mechanism of SOCS1 in JAK/STAT signaling pathway in exercised heart. Methods Male Sprague-Dawley rats were submitted to continuous graded treadmill running, then were sacrificed at 0, 1, 3, 5, 12 and 24 h respectively after the exercise. JAK1, JAK3 and SOCS1 expressions in myocardium were determined with immunohistochemistry. Results JAK1 expression significantly increased imme- diately after running in comparison with control group, peaked at 1 N 5 h, and remained high at 24 hr after exer- cise; in contrast, JAK3 and SOCS1 expressions significant decreased from 1 h to 5 h after running, then gradually back to sedentary level 12 h after exercise. Conclusion Acute exercise induced different responses of JAK1 and JAK3, which indicated the different functions of JAKs in exercised heart, SOCS1 may involve in regulating JAK/ STAT3 signal pathway in the exercised heart.
出处 《基础医学与临床》 CSCD 北大核心 2008年第6期575-578,共4页 Basic and Clinical Medicine
基金 北京市重点实验室开放实验室课题资助项目(2007-1)
关键词 运动 心肌 JAK酪氨酸蛋白激酶 细胞因子信号抑制因子1 exercise myocardium JAK SOCS1
  • 相关文献

参考文献10

  • 1Kurdi M, Booz GW. Can the protective actions of JAKSTAT in the heart be exploited therapeutically? Parsing the regulation of Interleukin-6-type cytokine signaling [ J ]. J Cardiovasc Phyarmaol, 2007, 50(2) :126- 141.
  • 2Haan C, Kreis S, Margue C, et al. Jaks and cytokine receptors -An intimate relationship [ J ]. Biochem Pharmacol, 2006, 72:1538 - 1546.
  • 3Rodig SJ, Meraz MA, White JM, et al. Disruption of the Jak1 gene demonstrates obligatory and nonredundant roles of the Jaks in cytokine-induced biologic responses [ J ]. Cell, 1998, 93:373 -383.
  • 4Ananthakrishnan R, Hallam K, Li Qin, et al. JAK-STAT pathway in cardiac ischemic stress [ J]. Vascul Pharmacol, 2005, 43(5) :353 -356.
  • 5Changelian PS, Flanagan ME, Ball DJ, et al. Prevention of organ allograft rejection by a specific Janus kinase 3 inhibitor [J]. Science, 2003, 302(5646): 875-878.
  • 6Kurdi M, Booz GW. Evidence that IL-6-type cytokine signaling in cardiomyocytes is inhibited by oxidative stress: parthenolide targets JAK1 activation by generating ROS [J]. J Cell Physiol, 2007, 212(2) :424 -431.
  • 7Duhe R J, Evans GA, Erwin RA, et al. Nitric oxide and thiol redox regulation of Janus kinase activity [ J ]. Proc Natl Acad Sci USA, 1998, 95:126- 131.
  • 8Navarrp-Areva; p A, Canavate C, Sanchez-del-Pino MJ. Myocardial and skeletal muscle aging and changes in oxidative stress in relationship to rigorous exercise training [ J ]. Mech Ageing Dev, 1999, 108 (3) :207 - 217.
  • 9Traverse JH, Nesmelov YE, Crampton M, et al. Measurement of myocardial free radical production during exercise using EPR spectroscopy [ J ]. Am J Physiol Heart Cire Physiol, 2006, 290 (6) : H2453 - 2458.
  • 10Krebs DL, Hilton DJ. SOCS proteins: negative regulators of cytokine signaling[J]. Stem Cell, 2001, 19(5) :378 - 387.

同被引文献30

引证文献2

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部