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Sirtuin 4 Regulates Lipopolysaccharide Mediated Leydig Cell Dysfunction
Author(s) -
Ramatchandirin Balamurugan,
Sadasivam Mohanraj,
Kannan Arun,
Prahalathan Chidambaram
Publication year - 2016
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25374
Subject(s) - apoptosis , leydig cell , lipopolysaccharide , sirtuin 1 , microbiology and biotechnology , endocrinology , sirtuin , medicine , cell , pathogenesis , biology , chemistry , downregulation and upregulation , gene , biochemistry , hormone , acetylation , luteinizing hormone
Bacterial lipopolysaccharide (LPS) is the most important contributing factor in pathogenesis of bacterial infection in male accessory glands; and it has shown to inhibit testicular steroidogenesis and induce apoptosis. The present study demonstrates that LPS causes mitochondrial dysfunction via suppression of sirtuin 4 (SIRT4); which in turn affects Leydig cell function by modulating steroidogenesis and apoptosis. LC‐540 Leydig cells treated with LPS (10µg/ml) showed impaired steroidogenesis and increased cellular apoptosis. The mRNA and protein expression of SIRT4 were decreased in LPS treated cells when compared to controls. The obtained data suggest that the c‐Jun N‐terminal kinase (JNK) activation suppresses SIRT4 expression in LPS treated Leydig cells. Furthermore, the overexpression of SIRT4 prevented LPS induced impaired steroidogenesis and cellular apoptosis by improving mitochondrial function. These findings provide valuable information that SIRT4 regulates LPS mediated Leydig cell dysfunction. J. Cell. Biochem. 117: 904–916, 2016. © 2015 Wiley Periodicals, Inc.