| First Author | Xu W | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 7403 |
| PubMed ID | 29743498 | Mgi Jnum | J:263114 |
| Mgi Id | MGI:6163369 | Doi | 10.1038/s41598-018-25427-3 |
| Citation | Xu W, et al. (2018) Calretinin Participates in Regulating Steroidogenesis by PLC-Ca(2+)-PKC Pathway in Leydig Cells. Sci Rep 8(1):7403 |
| abstractText | 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-PKCmicro (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. |
