Abstract
VIP is a peptide hormone capable of activating the cAMP/PKA pathway and modifying gonadal steroidogenic capacity. Less is known about the molecular mechanisms of VIP-mediated steroidogenesis and its role in regulating the steroidogenic acute regulatory protein (STAR). We examined the impact of VIP on STAR expression and function in immortalized (KK1) and primary mouse granulosa cells, where VIP strongly upregulated STAR expression and steroidogenesis. Inhibitors of the PKA and PKC pathways suggested that both are activated by VIP. VIP did not efficiently phosphorylate STAR (P-STAR); however, VIP together with cAMP-analogs that activate Type II PKA increased P-STAR and further increased steroidogenesis. Our results suggest that VIP-induced STAR expression and function in granulosa cells result from the preferential activation of Type I PKA. Furthermore, the PKA and PKC pathways appear to converge at regulating VIP-mediated Star transcription and translation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 93-103 |
| Number of pages | 11 |
| Journal | Molecular and Cellular Endocrinology |
| Volume | 328 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Oct 2010 |
Funding
This investigation was supported by NIH grant HD-17481 and with funds from the Robert A. Welch Foundation Grant B1-0028. The skilful technical assistance of Yuping Sun is greatly appreciated.
Keywords
- Granulosa cells
- STAR
- Steroidogenesis
- VIP
ASJC Scopus subject areas
- Endocrinology
- Molecular Biology
- Biochemistry