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PLoS One. 2009 Jun 2;4(6):e5765. doi: 10.1371/journal.pone.0005765.

Wnt5a increases cardiac gene expressions of cultured human circulating progenitor cells via a PKC delta activation.

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  • 1Institute of Cardiovascular Regeneration, Center for Molecular Medicine, JW Goethe University, Frankfurt, Germany.

Abstract

BACKGROUND:

Wnt signaling controls the balance between stem cell proliferation and differentiation and body patterning throughout development. Previous data demonstrated that non-canonical Wnts (Wnt5a, Wnt11) increased cardiac gene expression of circulating endothelial progenitor cells (EPC) and bone marrow-derived stem cells cultured in vitro. Since previous studies suggested a contribution of the protein kinase C (PKC) family to the Wnt5a-induced signalling, we investigated which PKC isoforms are activated by non-canonical Wnt5a in human EPC.

METHODOLOGY/PRINCIPAL FINDINGS:

Immunoblot experiments demonstrated that Wnt5a selectively activated the novel PKC isoform, PKC delta, as evidenced by phosphorylation and translocation. In contrast, the classical Ca(2+)-dependent PKC isoforms, PKC alpha and beta2, and one of the other novel PKC isoforms, PKC epsilon, were not activated by Wnt5a. The PKC delta inhibitor rottlerin significantly blocked co-culture-induced cardiac differentiation in vitro, whereas inhibitors directed against the classical Ca(2+)-dependent PKC isoforms or a PKC epsilon-inhibitory peptide did not block cardiac differentiation. In accordance, EPC derived from PKC delta heterozygous mice exhibited a significant reduction of Wnt5a-induced cardiac gene expression compared to wild type mice derived EPC.

CONCLUSIONS/SIGNIFICANCE:

These data indicate that Wnt5a enhances cardiac gene expressions of EPC via an activation of PKC delta.

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