Differential expression of microRNAs in luteinising hormone-treated mouse TM3 Leydig cells

Abstract

Testosterone is primarily produced by Leydig cells of the mammalian male gonads. The cellular functions of Leydig cells are regulated by the hypothalamus-pituitary-gonad axis, whereas the microRNA (miRNA) changes of LH-treated Leydig cells are unknown. Mouse TM3 Leydig cells were treated with LH, and deep sequencing showed that 29 miRNAs were significantly different between two groups (fold change of >1.5 or <0.5, p < .05), of which 27 were upregulated and two were downregulated. The differential expression of miR-29b-3p, miR-378b, miR-193b and miR-3695 was confirmed by quantitative real-time polymerase chain reaction. Bioinformatic analysis revealed that miRNAs regulated a large number of genes with different functions. Pathway analysis indicated that miRNAs were involved in the Wingless and INT-1, adenosine 5'-monophosphate-activated protein kinase, NF-kappa B and Toll-like receptor signalling pathways. Results showed that miRNAs might be involved in the regulation of LH to Leydig cells.

Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line

“…The miRNA maturation process involved in the nuclear processing of primary miRNA by DROSHA, nuclear export of precursor miRNA (pre- miRNA) by exportin 5, and cytoplasmic processing of pre- miRNA by DICER [15]. Recent studies showed that the differential expression of miRNAs in mouse Leydig cells was discovered by the addition of the brain-derived neurotrophic factor and luteinizing hormone during the cultivation of TM3 cells [16,17]. These studies show that miRNAs may be involved in the regulation of hormones in certain physiological functions of mouse Leydig cells.…”

microRNA-378b regulates ethanol-induced hepatic steatosis by targeting CaMKK2 to mediate lipid metabolism

“…MiRNAs have been shown to regulate lipid metabolism directly or indirectly through epigenetic mechanisms [ 17 ]. Previous research showed that miR-378b was markedly decreased in plasma from coronary heart disease (CHD) patients, the livers from diet-induced obese SD rats under hypoxic training and neurofibromatosis 1 (NF1) patient brain specimens [ 28 , 29 ], and miR-378b expression was also significantly increased in luteinizing hormone-treated mouse TM3 Leydig cells [ 30 ]. In this paper, we took the lead in finding that miR-378b was up-regulated by EtOH, and miR-378b was involved in hepatic lipid dysfunction induced by EtOH.…”