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Regulation of cytochrome P450 1B1 expression by luteinizing hormone in mouse MA-10 and rat R2C Leydig cells: role of protein kinase A.

Authors: Deb, S  Bandiera, SM 
Citation: Deb S and Bandiera SM, Biol Reprod. 2011 Jul;85(1):89-96. doi: 10.1095/biolreprod.110.088971. Epub 2011 Mar 9.
Pubmed: (View Article at PubMed) PMID:21389345
DOI: Full-text: DOI:10.1095/biolreprod.110.088971

In the present study, we investigated the signaling pathway involved in luteinizing hormone (LH)-mediated regulation of testicular CYP1B1 in mouse MA-10 and rat R2C Leydig cells. CYP1B1 mRNA and protein levels were measured in MA-10 and R2C cells treated with LH and protein kinase activators or inhibitors. Treatment with LH or 8-bromo-cAMP, a protein kinase A (PRKA) activator, increased CYP1B1 expression and PRKA activity in a concentration-dependent manner in both cell lines, albeit to different extents. Treatment with 8-(4-chlorophenylthio)adenosine-3',5'-cyclic monophosphorothioate, Rp-isomer, a PRKA inhibitor, decreased basal CYP1B1 expression and attenuated LH-elicited increases in CYP1B1 mRNA and protein levels and PRKA activity. In contrast, treatment with a protein kinase G activator or an inhibitor of protein kinase C had no effect on basal or LH-induced CYP1B1 expression in MA-10 or R2C cells. Collectively, the results identify PRKA as the major signaling pathway involved in the LH-mediated regulation of testicular CYP1B1 expression in Leydig tumor cells.


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CRRD Object Information
CRRD ID: 7800737
Created: 2014-01-20
Species: All species
Last Modified: 2014-01-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.