| Autor: |
Chen, Yabing1,2, Wang, Jing1,2, Zhang, Qin1,2, Xiang, Zou3, Li, Dongmei1,2, Han, Xiaodong1,2 hanxd@nju.edu.cn |
| Předmět: |
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| Zdroj: |
Environmental Pollution. Oct2017, Vol. 229, p964-975. 12p. |
| Abstrakt: |
Microcystin-leucine arginine (MC-LR) causes testicular inflammation and hinders spermatogenesis. However, the molecular mechanisms underlying the immune responses to MC-LR in the testis have not been elucidated in detail. In this study, we show that MC-LR induced immune responses in Sertoli cells (SC), germ cells (GC), and Leydig cells (LC) via activating phosphatidylinositol 3-kinase (PI3K)/AKT/nuclear factor kappa B (NF- κ B), resulting in the production of pro-inflammatory cytokines and chemokines including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and chemokine (C-X-C motif) ligand 10 (CXCL10). The observed effects were attributed to reduced activity of protein phosphatases 2A (PP2A) as a result of binding of MC-LR to the catalytic subunit of PP2A in SC and GC. By contrast, innate immune responses were triggered by Toll-like receptor 2 (TLR2) in LC because MC-LR could not enter into the LC and subsequently inhibit the PP2A activity. PI3K/AKT/NF- κ B were also activated in SC, GC, and LC in vivo , with the enrichment of TNF-α, IL-6, MCP-1, and CXCL10 in the testis. Following chronic exposure, MC-LR-treated mice exhibited decreased sperm counts and abnormal sperm morphology. Our data demonstrate that MC-LR can activate innate immune responses in testicular cells, which provides novel insights to explore the mechanism associated with MC-LR-induced orchitis. [ABSTRACT FROM AUTHOR] |
| Databáze: |
GreenFILE |
| Externí odkaz: |
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Full Text from ScienceDirect