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Differential regulation of TNF receptor 1 and receptor 2 in adiponectin expression following myocardial ischemia
  • 期刊名称:《生理通讯》
  • 分类:R4[医药卫生—临床医学]
  • 作者机构:[1]Department of Physiology, Shanxi Medical University, Taiyuan 030001, China, [2]Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA 19107, United States, [3]Department of Anesthesiology, First Affiliated Hospital, Shanxi Medical University, Taiyuan 030001, China, [4]Department of Cardiology, Fourth Military Medical University, Xian 710032, China, [5]Center for Translational Medicine, Temple University Medical School, Philadelphia, PA 19107, United States
  • 相关基金:Acknowledgment This research was supported by grants from the American Diabetes Association (1-11-JF56) and the Natural Science Foundation of China (30900592, 81170199) (to YJW) , and NIH ( HL-63828, HL-096686 ) and American Diabetes Association (7-11-BS-93) (to XLM).
中文摘要:

2013年10月12—13日中国生理学会张锡钧基金会第十二届全国青年优秀生理学学术论文交流会在湖南长沙顺利召开。由各省生理学会推荐的37名参赛选手的论文参与评选,会议展示了选手们近3年来在生理学研究方面所取得的最新研究成果。经过专家对参评者论文和现场报告的综合评判,评出一等奖、二等奖、三等奖、特别奖、最佳表达奖、最佳答辩奖和最佳图标奖共11名。从2013年第6期开始,《生理通讯》将陆续转载获奖者的参评论文各一篇,以飨读者。

英文摘要:

Background: In vitro experiments demonstrate that adiponectin, a cardioprotective cytokine, is inhibited by tumor necrosis factor-alpha (TNFtx) . However, the role of TNFet in post-myocardial infarction ( post-MI ) adiponectin reduction remains unclear. More importantly, the TNF receptor type (TNFR1 or TNFR2) responsible for TNFa-mediated suppression of adiponectin production is unknown. The current study determined the role of TNFtx in post-myocardial infarction (post-MI) adiponectin reduction, and identified the receptor type responsible for TNF~- mediated suppression of adiponectin production. Methods and results: Adult male wild type (WT) and three knockout variety (TNFa-/-, TNFR1-/-, and TNFR2-/-) mice were subjected to MI via coronary artery occlusion. Histological and biochemical analyses were performed 3 and 7 days post-MI. In WT mice, MI significantly increased plasma TNF~, reduced adipocyte adiponectin mRNA, and decreased plasma adiponectin levels. TNFa deletion had no significant effect upon basal adiponectin level, and partially restored adiponectin expression/production post-MI (P〈 0.01 vs. WT) . Basal adiponectin levels were significantly increased in TNFR1-/- (P〈0.05 vs. WT), and unchanged in TNFR2-/-rnice. Importantly, suppressed adiponectin expression/production by MI or TNFa administration was markedly decreased by TNFR1 deletion (P 〈 0.01 vs. WT), but exacerbated by TNFR2 deletion (P 〈 0.05 vs. WT). Mechanistically, TNFR1 knockout significantly inhibited, whereas TNFR2 knockout further enhanced TNFa-induced mRNA and protein expression of ATF3, a transcriptional factor known to significantly inhibit adiponectin expression. Conclusion: Our study demonstrates that TNFa overproduction is responsible for reduced adiponectin expression/production following MI. Furthermore, we show that TNFR1/TNFR2 exerts opposite effects upon adiponectin expression/ production via differential regulation of ATF3.

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