Where are the theca cells from: the mechanism of theca cells derivation and differentiation.

Mammalian follicles are composed of oocytes, granulosa cells, and theca cells. Theca cells form in the secondary follicles, maintaining follicular structural integrity and secreting steroid hormones. Two main sources of theca cells exist: Wilms tumor 1 positive (Wt1) cells native to the ovary and Gli1 mesenchymal cells migrated from the mesonephros. Normal folliculogenesis is a process where oocytes, granulosa cells, and theca cells constantly interact with and support each other through autocrine and paracrine mechanisms. The proliferation and differentiation of theca cells are regulated by oocyte-derived factors, including growth development factor 9 and bone morphogenetic protein 15, and granulosa cell-derived factors, including desert hedgehog, Indian hedgehog, kit ligand, insulin-like growth factor 1, as well as hormones such as insulin and growth hormones. Current research on the origin of theca cells is limited. Identifying the origin of theca cells will help us to systematically elaborate the mechanisms of follicular formation and development.

G protein-coupled estrogen receptor is involved in the anti-inflammatory effects of genistein in microglia.

BACKGROUND: Genistein (GEN), a phytoestrogen that is extracted from leguminous plants, can bind to estrogen receptor and exert biological effects. G protein-coupled estrogen receptor (GPER), a novel membrane estrogen receptor, has been reported to be involved in the anti-inflammatory process. In the present study, using BV2 microglial cell line and primary microglial culture, we evaluated the involvement of GPER in the anti-inflammatory effects of genistein against lipopolysaccharide (LPS)-induced microglia activation. METHODS: The anti-inflammatory effects of genistein were investigated in LPS-induced microglial activation in murine BV2 microglial cell line and primary microglial culture. Anti-inflammatory properties of genistein were determined by MTT, real time PCR, ELISA and western blot analysis. The pharmacological blockade and lentivirus-mediated siRNA knockdown of GPER were used to study the underlying mechanism. RESULTS: The results showed that genistein exerted inhibitory effects on LPS-induced expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide (iNOS), tumor necrosis factor-α (TNF-α), interleukin-1 ß (IL-1ß) and interleukin-6 (IL-6). Pre-treatment with GPER antagonist G15 could significantly block the anti-inflammatory effects of genistein. Moreover, the inhibitory effects of genistein on LPS-induced activation of MAPKs and NF-κB signaling pathways could also be blocked by G15. Lentivirus-mediated siRNA knockdown of GPER significantly inhibited the anti-inflammatory effects of genistein in BV2 cells. Further study revealed that genistein treatment could increase the gene and protein expressions of GPER in BV2 cells. CONCLUSION: Taken together, these data provide the first evidence that genistein exerts anti-inflammatory effects in microglial cells via GPER activation. These beneficial effects of genistein may represent a new strategy for the treatment of neuroinflammatory diseases.