| First Author | Li J | Year | 2015 |
| Journal | Sci Rep | Volume | 5 |
| Pages | 9720 | PubMed ID | 25988316 |
| Mgi Jnum | J:243970 | Mgi Id | MGI:5912749 |
| Doi | 10.1038/srep09720 | Citation | Li J, et al. (2015) Robo1/2 regulate follicle atresia through manipulating granulosa cell apoptosis in mice. Sci Rep 5:9720 |
| abstractText | Secreted Slit proteins and their Roundabout (Robo) receptors act as a repulsive cue to prevent axons from migrating to inappropriate locations during the development of the nervous system. Slit/Robo has also been implicated in reproductive system development, but the molecular mechanism of the Slit/Robo pathway in the reproductive system remains poorly understood. Using a transgenic mouse model, we investigated the function of the Slit/Robo pathway on ovarian follicle development and atresia. We first demonstrated that more offspring were born to mice with a partial knockout of the Robo1/2 genes in mice. We next showed that Robo1 and Robo2 are strongly expressed in ovarian granulosa cells. Apoptosis in granulosa cells was reduced when Robo1/2 were partially knocked out, and this observation was further verified by in vitro Robo1/2 knockout experiments in mouse and human granulosa cells. We also found that ovarian angiogenesis was enhanced by a partial lack of Robo1/2 genes. In summary, our data suggest that the Slit/Robo pathway can impact follicle development and atresia by influencing granulosa cell apoptosis. |
