MECHANISMS OF HORMONE AND GROWTH-FACTOR ACTION IN THE BOVINE CORPUS-LUTEUM

The binding of hormones and growth factors to their cell surface recep tors leads to an orderly cascade of events leading to activation of cy toplasmic effector molecules. The mechanism of action of luteinizing h ormone involves the stimulation of multiple signal transduction effect or systems including adenylyl cyclase and inositol phospholipid-specif ic phospholipase C (PLC). This results in the formation of second mess engers that activate cAMP-dependent. Ca2+-dependent and lipid-dependen t protein kinases. Prostaglandin F-2 alpha activates PLC which increas es intracellular calcium and activates protein kinase C. This results in the activation of a series of protein kinases in the mitogen-activa ted protein (MAP) kinase cascade, leading to the activation of nuclear transcription factors c-fos and c-jun. Hormone responsive effector sy stem, therefore, operate by activating families of protein kinases whi ch regulate cell metabolism secretion, and gene transcription. Growth factors activate specific receptor protein tyrosine kinases which recr uit additional signaling molecules (phospholipase C gamma, phosphatidy linositol 3-kinase, Shc, Grb2, etc.) initiating a cascade of events me diated via MAP kinases. The signaling pathways activated by hormones i nteract or cross talk with the signaling pathways activated by growth factors. The diversity of cellular signaling mechanisms elicited by ho rmones and the potential for interactions with signals generated by gr owth factor receptor tyrosine kinases, may allow fine tuning of cellul ar responses during the life span of the corpus luteum.