Effect of Tumor Necrosis Factor-αon Expression of Skeletal Muscle Proteasome Subunit C2 in Rats with Chronic Obstructive Pulmonary Disease_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

ZHANG Yue ,  XU Weiguo , LUO Yong , HAN Fengfeng , YANG Tianyun , CHEN Yinchun

Department of Respiratory Diseases, Xinhua Hospital, School of Medicine,Shanghai Jiaotong University. Shanghai, 200092, China Corresponding Author: XU Wei-guo, E-mail: xwg_xinhua@ yahoo. com;

Corresponding author：

XU Weiguo, Email: xwg_xinhua@yahoo.com

Keywords：

Chronic obstructive pulmonary disease; Tumor necrosis factor-α; Skeletalmuscle protein; Ubiquitin-dependent proteolytic system; Proteasome subunit C2

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Objective To study the effect of tumor necrosis factor-α( TNF-α) onhypermetabolism of skeletal muscle protein in rats with chronic obstructive pulmonary disease ( COPD) and explore its underlying mechanism. Methods Forty-five SD rats were randomly divided into a normal control group, a COPD group and a COPD + TNF-α group, with 15 rats in each group. COPD model was established by passive cigarette smoking in COPD group and COPD + TNF-αgroup. Then the extensor digitorium longus muscles ( EDL) were dissected and incubated in vitro muscle incubation system with adequate oxygen supply. The EDL were either cultured with or without recombinant rat TNF-α( 10 μg/L) . The mRNA and protein expressions of proteasome subunit C2 in EDL were quantified by real-time quantitative PCR and Western blot analysis, respectively. Results The mRNA and protein expressions of proteasome subunit C2 were both significant higher in the COPD group and COPD + TNF-αgroup than those in the normal control group( P lt;0. 01 or 0. 05) . The COPD+TNF-αgroup had higher expression of proteasome subunit C2 mRNA than that in the COPD group( P lt; 0. 01) , whereas the protein expression was not significantly different( P gt; 0. 05) . Conclusion Incresed proteolytic metabolism in skeletal muscle in COPD might be regulated by TNF-αactivated ubiquitin-dependent pathway.

Citation： ZHANG Yue,XU Weiguo,LUO Yong,HAN Fengfeng,YANG Tianyun,CHEN Yinchun. Effect of Tumor Necrosis Factor-αon Expression of Skeletal Muscle Proteasome Subunit C2 in Rats with Chronic Obstructive Pulmonary Disease. Chinese Journal of Respiratory and Critical Care Medicine, 2009, 09(5): 436-440. doi: Copy

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28.	年欧洲呼吸学会年会慢性阻塞性肺疾病研究进展. 中国呼吸与危重监护杂志, 2004, 3: 413-415.

1. Man WD, Moxham J, Polkey MI. Magnetic stimulation for the measurement of respiratory and skeletal muscle function. Eur Respir J, 2004, 24: 846-860.
2. 王曾礼. 更新对慢性阻塞性肺疾病认识的观念. 中国呼吸与危重监护杂志, 2007, 6: 401-402.
3. 白冲. 慢性阻塞性肺疾病的危险因素、流行情况及未来发展趋势. 中国呼吸与危重监护杂志,2007, 6: 403-405.
4. Schols AM. Nutritional and metabolic modulation in chronic obstructive pulmonary disease management. Eur Respir J Suppl, 2003, 46: 81s-86s.
5. 杨天芸, 徐卫国, 罗勇, 等. 慢性阻塞性肺病大鼠骨骼肌蛋白降解的变化. 上海交通大学学报( 医学版) , 2008, 28: 525-527.
6. Creutzberg EC, Schols AM, Weling-Scheepers CA, et al. Characterization of nonresponse to high caloric oral nutritional therapy in depleted patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2000, 161: 745-752.
8. 李红梅, 崔德健, 佟欣, 等. 熏香烟加气管注内毒素和单纯熏香烟法建立大鼠COPD 模型. 中国病理生理杂志, 2002, 18: 808-812.
9. Celli BR, MacNee W, ATS /ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS /ERS position paper. Eur Respir J, 2004, 23: 932-946.
10. 姚婉贞, 陈亚红.
11. , No.
12. Jagoe RT, Engelen MP. Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease. Eur Respir J Suppl, 2003, 46: 52s-63s.
13. Rutten EP, Franssen FM, Engelen MP, et al. Greater whole-body myofibrillar protein breakdown in cachectic patients with chronic obstructive pulmonary disease. Am J Clin Nutr, 2006, 83: 829-834.
14. Bargon J, Müller U, Buhl R. COPD, a systemic disease--nutritional approaches. Med Klin( Munich) , 2004, 99: 719-726.
15. 高福生, 潘全, 李淑兰, 等. 慢性阻塞性肺疾病患者营养状态对运动耐力及通气氧耗的影响. 中国呼吸与危重监护杂志, 2004, 中国呼吸与危重监护杂志2009 年9 月第8 卷第5 期Chin J Respir Crit Care Med, September 2009, Vol.
16. Gao M, Karin M. Regulating the regulators: control of protein ubiquitination and ubiquitin-like modifications by extracellular stimuli. Mol Cell, 2005, 19: 581-593.
17. Taillandier D, Combaret L, Pouch MN, et al. The role of ubiquitinproteasome- dependent proteolysis in the remodelling of skeletal muscle. Proc Nutr Soc, 2004, 63: 357-361.
18. McKinnell IW, Rudnicki MA. Molecular mechanisms of muscle atrophy. Cell, 2004, 119: 907-910.
19. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2 - △△ Ct method. Methods, 2001, 25: 402-408.
20. Adams V, Mangner N, Gasch A, et al. Induction of MuRF1 is essential for TNF-alpha-induced loss of muscle function in mice. J Mol Biol, 2008, 384: 48-59.
21. Schols AM. Pulmonary cachexia. Int J Cardiol, 2002, 85: 101-110.
22. Van Helvoort HA, Heijdra YF, Thijs HM, et al. Exercise-induced systemic effects in muscle-wasted patients with COPD. Med Sci Sports Exerc, 2006, 38: 1543-1552.
23. Sevenoaks MJ, Stockley RA. Chronic Obstructive Pulmonary Disease, inflammation and co-morbidity--a common inflammatory phenotype? Respir Res, 2006, 7 : 70 .
24. Eid AA, Ioneseu AA, Nixon LS. Inflammatory Response and Body Composition in Chronic Obstructive Pulmonary Disease. AmJRespir Crit Care Meel Vol, 2001, 164: 1414-1418.
25. 徐卫国, 罗勇, 吴靖川, 等. 不同营养状态COPD 肿瘤坏死因子- α测定及其临床意义. 中国实用内科杂志, 1999, 19: 654-655.
26. Ryther RCC, Flynt AS, Phillips 3rd JA, et al. siRNA therapeutics: big potential from small RNAs. Gene Ther, 2005, 12: 5-11.
27. Tisdale MJ. The ubiquitin-proteasome pathway as a therapeutic target for muscle wasting. J Support Oncol, 2005, 3: 209-217.
28. 年欧洲呼吸学会年会慢性阻塞性肺疾病研究进展. 中国呼吸与危重监护杂志, 2004, 3: 413-415.

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