دورية أكاديمية
Mitofusin 2 Promotes Apoptosis of CD4+ T Cells by Inhibiting Autophagy in Sepsis
العنوان: | Mitofusin 2 Promotes Apoptosis of CD4+ T Cells by Inhibiting Autophagy in Sepsis |
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المؤلفون: | Lan Ying, Guang-Ju Zhao, You Wu, He-Liang Ke, Guang-Liang Hong, Hui Zhang, Ning Dong, Yao Wu, Yong-Ming Yao, Zhong-Qiu Lu |
المصدر: | Mediators of Inflammation, Vol 2017 (2017) |
بيانات النشر: | Wiley, 2017. |
سنة النشر: | 2017 |
المجموعة: | LCC:Pathology |
مصطلحات موضوعية: | Pathology, RB1-214 |
الوصف: | Apoptosis of CD4+ T cells is a primary pathophysiological mechanism of immune dysfunction in the pathogenesis of sepsis. Mitofusin 2 (Mfn2), an integral mitochondrial outer membrane protein, has been confirmed to be associated with cellular metabolism, proliferation, and apoptosis. The function of Mfn2 in CD4+ T cell apoptosis in sepsis is poorly understood. Here, we discovered increased in vivo Mfn2 expression, autophagy deficiency, and elevated cell apoptosis in murine splenic CD4+ T cells after cecal ligation and puncture (CLP). We also observed almost identical results in splenic CD4+ T cells upon lipopolysaccharide (LPS) stimulation in vitro. Furthermore, overexpression of Mfn2 resulted in impaired autophagy and increased apoptosis in Jurkat cells. Pharmacological inhibition of autophagy with 3-methyladenine enhanced Mfn2 overexpression-induced cell apoptosis. In addition, overexpression of Mfn2 downregulated phorbol myristate acetate (PMA)/ionomycin-, rapamycin- and starvation-induced autophagy in Jurkat T cells. Taken together, these data indicate a critical role of Mfn2 in CD4+ T cell apoptosis in sepsis and the underlying mechanism of autophagy deficiency. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 0962-9351 1466-1861 |
Relation: | https://doaj.org/toc/0962-9351; https://doaj.org/toc/1466-1861 |
DOI: | 10.1155/2017/4926205 |
URL الوصول: | https://doaj.org/article/73d339c92d40462fb437dc9a993ee775 |
رقم الأكسشن: | edsdoj.73d339c92d40462fb437dc9a993ee775 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 09629351 14661861 |
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DOI: | 10.1155/2017/4926205 |