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Insulin and heregulin-beta1 upregulate guanylyl cyclase C expression in rat hepatocytes: reversal by phosphodiesterase-3 inhibition.

Scheving LA, Russell WE
Cell Signal. 2001 13 (9): 665-72

PMID: 11495724 · DOI:10.1016/s0898-6568(01)00179-6

Guanylyl cyclase C (GC-C) is the receptor for the hormones guanylin and uroguanylin. Although primarily expressed in the rat intestine, GC-C is also expressed in the liver during neonatal or regenerative growth or during the acute phase response. Little is known about the hepatic regulation of GC-C expression. The influence of various hepatic growth or acute phase regulators on GC-C expression was evaluated by immunoblot analysis of protein from primary rat hepatocytes grown in a serum-free medium. Insulin and heregulin-beta1 strongly stimulated GC-C expression by 24 h of cell culture. Several different hormones and agents suppressed this action, including transforming growth factor beta (TGF-beta), as well as inhibitors of phosphatidylinositol 3-kinase (PI-3-kinase) and phosphodiesterase 3 (PDE-3, an insulin- and PI-3-kinase-dependent enzyme). The compartmental downregulation of cAMP levels by PDE-3 may be a critical step in the hormonal action that culminates in GC-C synthesis.

MeSH Terms (25)

3',5'-Cyclic-AMP Phosphodiesterases Animals Cells, Cultured Cyclic AMP Cyclic Nucleotide Phosphodiesterases, Type 3 Dexamethasone Drug Antagonism Drug Synergism Enzyme Inhibitors Glucagon Guanylate Cyclase Hepatocytes Insulin Male Neuregulin-1 NG-Nitroarginine Methyl Ester Nitric Oxide Synthase Nitric Oxide Synthase Type II Phosphatidylinositol 3-Kinases Rats Rats, Sprague-Dawley Receptors, Enterotoxin Receptors, Guanylate Cyclase-Coupled Receptors, Peptide Up-Regulation

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