Calretinin Participates in Regulating Steroidogenesis by PLC-Ca2+-PKC Pathway in Leydig Cells

作者：Wendan Xu, Qian Zhu, Shan Liu, Xiaonan Dai, Bei Zhang, Chao Gao, Li Gao, Jiayin Liu, Yugui Cui · 发表于：Scientific Reports · 年份：2018 · DOI：10.1038/s41598-018-25427-3 · 被引用次数：26 · 研究领域：Sperm and Testicular Function、Retinoids in leukemia and cellular processes、Hormonal and reproductive studies

Abstract Calretinin, a Ca 2+ -binding protein, participates in many cellular events. Our previous studies found the high expression of calretinin in testicular Leydig cells. In this study, (MLTC-1 cells were infected with LV-calb2, R2C cells with LV-siRNA-calb2. The primary mouse Leydig cells were also used to confirm those data from cell lines. Testosterone level was significantly higher in the MLTC-1 cells with over-expressed calretinin than in the control, while progesterone was lower in the R2C cells in which down-regulated calretinin. The expressions of StAR changed in synchrony with hormones. Cytoplasmic Ca 2+ level was significantly increased when calretinin was over-expressed. When MLTC-1 cells were infected with LV-calb2 and then stimulated using Clopiazonic, a Ca 2+ -releasing agent, testosterone was significantly increased. Interestingly, the expression levels of PLC, p-PKCµ (PKD), p-MARCKS and CREB, were significantly increased in the MLTC-1 cells with over-expressed calretinin, while PLC, p-PKD, p-MARCKS, MARCKS and CREB were decreased in the R2C cells with down-regulated calretinin. We also observed the increased expression of calretinin up-regulated testosterone production and the expressions of StAR and PLC in primary mouse Leydig cells. So, calretinin as a Ca 2+ -binding protein participates in the regulation of steroidogenesis via the PLC-Ca 2+ -PKC pathway in Leydig cells.