Hypertrophic effects of urocortin homologous peptides are mediated via activation of the Akt pathway

Anastasios Chanalaris, Kevin M. Lawrence, Paul A. Townsend, Sean Davidson, Yalda Jashmidi, Anastasis Stephanou, Richard D. Knight, Sheau Y. Hsu, Aaron J W Hsueh, David S. Latchman

    Research output: Contribution to journalArticlepeer-review


    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. © 2005 Published by Elsevier Inc.
    Original languageEnglish
    Pages (from-to)442-448
    Number of pages6
    JournalBiochemical and Biophysical Research Communications
    Issue number2
    Publication statusPublished - 11 Mar 2005


    • Akt
    • Cardiomyocytes
    • Hypertrophy
    • MAPK
    • Natriuretic peptides
    • Stresscopin
    • Stresscopin related peptide
    • Urocortin


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