Fig. 2

Functions of FSH signaling in SC proliferation, differentiation and apoptosis. Binding of FSH to FSHR recruits Gɑs to FSHR, activating AC. AC transforms ATP into cAMP, and cAMP binds to regulatory subunits of PKA to release catalytic subunits of PKA. Activated PKA induces the expression of c-Myc and Cyclin D1 to promote SC proliferation (red). c-Myc expression is also upregulated by the PI3K/Akt/mTOR pathway. The cAMP/PKA/ERK pathway leads to the expression of Cyclin D1 only during SC proliferation. Through an unknown pathway, FSH induces the expression of HIF2 to promote c-Myc and Cyclin D1 expression. Moreover, inter-SC junction dynamics are also mediated by FSH signaling (green). FSH induces tPA expression via a cAMP/PKA-dependent pathway and three components of the BTB, N-cadherin, ɑ6β1-integrin and claudin 11, through an unknown pathway. Combined with testosterone, FSH stimulates Gja expression via the Wnt3 pathway. Additionally, FSH participates in SC differentiation (blue). Klf4, NF-κB and ASNS expression are mediated by the cAMP/PKA signaling pathway. HIF1 and Aqp8 expression are mediated by an unknown pathway. HIF1 mainly participates in the glycolytic pathway, and Aqp8 is important for water balance. Finally, the cAMP/PKA-mediated balance of FAAH and DAX1 maintains normal SC apoptosis (orange). The dotted line represents an unknown mechanism. For more information, please see the main text