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The UCN homologues SCP and SRP bind specifically to the CRFR2 receptor, whereas UCN binds to both CRFR1 and CRFR2. We have previously demonstrated that all three peptides are cardioprotective, and both the Akt and MAPK p42/44 pathways are essential for this effect. Here we tested the hypertrophic effects of these peptides. We examined the effects of the peptides on cell area, protein synthesis, and induction of the natriuretic peptides ANP and BNP. All three peptides were able to increase all the markers of hypertrophy examined, with SCP being the most potent of the three, followed by UCN and SRP last. In addition, we provide a mechanism of action for the three peptides and show that Akt phosphorylation is important for their hypertrophic action, whereas MAPK p42/44 is not involved in this effect.

Original publication

DOI

10.1016/j.bbrc.2005.01.001

Type

Journal article

Journal

Biochem Biophys Res Commun

Publication Date

11/03/2005

Volume

328

Pages

442 - 448

Keywords

Animals, Animals, Newborn, Cell Size, Cells, Cultured, Corticotropin-Releasing Hormone, Gene Expression Regulation, Hypertrophy, Myocytes, Cardiac, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Rats, Rats, Sprague-Dawley, Signal Transduction, Urocortins