Lipopolysaccharide-induced expression of FAS ligand in cultured immature boar sertoli cells through the regulation of pro-inflammatory cytokines andmiR-187
Autor: | Hong-Yan Luo, Xian-Zhong Wang, Yi Wang, Jia-Hua Zhang, Jiao Jiao Zhang, Wei-Rong Yang |
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Rok vydání: | 2015 |
Předmět: |
endocrine system
medicine.medical_specialty Lipopolysaccharide Cell Biology Biology Sertoli cell Fas ligand Proinflammatory cytokine Cell biology chemistry.chemical_compound medicine.anatomical_structure Endocrinology chemistry Apoptosis Internal medicine Genetics medicine Tumor necrosis factor alpha Germ cell Developmental Biology Transforming growth factor |
Zdroj: | Molecular Reproduction and Development. 82:880-891 |
ISSN: | 1040-452X |
DOI: | 10.1002/mrd.22534 |
Popis: | Lipopolysaccharide (LPS) induces germ cell apoptosis, but its mechanism of action is not clear. One possibility is that LPS regulates the expression of FAS ligand (FASLG) in Sertoli cells, which will then influence germ cell apoptosis. In this study, LPS reduced the viability of cultured, immature boar Sertoli cells in a time- and dose-dependent manner; enhanced the production of pro-inflammatory cytokines including tumor necrosis factor α (TNFA), interleukin-1β (IL1B), nitric oxide (NO), and transforming growth factor-β (TGFB); and increased the expression of FASLG in a dose-dependent manner. While 10 μg/ml LPS enhanced the expression of FASLG, reduced cell cycle progression, and impaired the ultrastructure of Sertoli cells, this dose did not induce apoptosis. LPS also had no effect on the activity or expression of matrix metalloproteinases 2 or 9 (MMP2 or MMP9). In contrast, the expression of ssc-miR-187 increased following LPS challenge, and inhibition of ssc-miR-187 blocked LPS-induced expression of FASLG. Our results therefore suggest that LPS reduces the viability of and enhances FASLG expression in cultured, immature boar Sertoli cells through elevated secretion of TNFA, IL1B, NO, and TGFB as well as through the regulation of ssc-miR-187 potency. |
Databáze: | OpenAIRE |
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