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Toxins 2016, 8(9), 260; doi:10.3390/toxins8090260

miR-541 Contributes to Microcystin-LR-Induced Reproductive Toxicity through Regulating the Expression of p15 in Mice

1,2,†
,
1,2,†
,
1,2
,
3
,
1,2,* and 1,2,*
1
Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, 22 Hankou Road, Nanjing 210093, Jiangsu, China
2
Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, 22 Hankou Road, Nanjing 210093, Jiangsu, China
3
Department of Health Technology and Informatics, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, China
*
Authors to whom correspondence should be addressed.
Academic Editors: Lesley V. D’Anglada, Elizabeth D. Hilborn and Lorraine C. Backer
Received: 19 June 2016 / Accepted: 31 August 2016 / Published: 6 September 2016
(This article belongs to the Collection Freshwater HABs and Health in a Changing World)
View Full-Text   |   Download PDF [8372 KB, uploaded 6 September 2016]   |  

Abstract

Microcystin-leucine arginine (MC-LR) is a harmful cyanotoxin produced by cyanobacteria. MC-LR can exert endocrine-disrupting activities in many organisms. We have previously demonstrated that MC-LR exerts both acute and chronic reproductive toxicity in male mice, resulting in a decline in sperm quality and damage to testicular structure. Moreover, we also observed extensive alterations in a panel of microRNAs in spermatogonial cells after exposure to MC-LR. In this study, we have confirmed that miR-541 was significantly increased both in GC-1 cells (in vitro) and in mouse testes (in vivo) after exposure to MC-LR. Our data support that p15 was the target gene of miR-541. Increase in miR-541 led to a reduction of p15 and murine double minute2 (MDM2), promoting the activation of p53 signaling and MC-LR-mediated cell apoptosis. Moreover, cells responded to MC-LR with reduced viability and increased apoptosis. Consistently, inhibiting miR-541 could upregulate the expression of p15 and MDM2, resulting in the downregulation of phospho-p53. Downregulation of miR-541 promoted cell viability by reducing MC-LR-induced cell apoptosis. In conclusion, we demonstrate here a crucial role for miR-541 in MC-LR-induced toxic effects on the reproductive system, in an attempt to provide a rational strategy for the diagnosis and treatment of MC-LR-induced impairment in the reproductive system. View Full-Text
Keywords: MC-LR; miR-541; p15; male reproduction; apoptosis MC-LR; miR-541; p15; male reproduction; apoptosis
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Meng, X.; Zhang, L.; Chen, X.; Xiang, Z.; Li, D.; Han, X. miR-541 Contributes to Microcystin-LR-Induced Reproductive Toxicity through Regulating the Expression of p15 in Mice. Toxins 2016, 8, 260.

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