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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: J Mol Cell Cardiol. 2009 May;46(5):728–738. doi: 10.1016/j.yjmcc.2009.01.017

Figure 7. PKC activity is essential for TB4 induced epicardial activation in adult mice in vivo.

Figure 7

A, Bisindolylmaleinimide-I alters capillary formation of HCECs and inhibits adult epicardial cell transformation on matrigel. a-h, HCECs transform to irregular, rounded (c,d black arrowheads) sm α- actin positive cells (g,h white arrowheads) when treated with PKC inhibitor. i-l, Bisindolylmaleinimide-I inhibits adult epicardial cell transformation on matrigel (k,l black arrowheads point at non-transformed cell groups). B. Immunohistochemical analyses with anti-sm α-actin (a-d) and anti-p-Marcks (e-h) antibodies show reduced epicardial thickening and inhibition of capillary outgrowths (c,g white arrowheads) in TB4+PKC inhibitor treated adult hearts (c,g) when compared to TB4 and no inhibitor treated controls (d,h). Decrease in p-Marcks expression indicated sufficient reduction of PKC activity in the inhibited control hearts (h). Administration of Bisindolylmaleinimide-I itself does not alter the adult mouse epicardium in vivo (d,h). i-j, Bisindolylmaleinimide-I significantly suppresses the number of capillaries (i) and sm 28-actin positive cells (j) in the non infarcted remote areas of TB4 treated hearts (n=6). k-l, Inhibition of PKC activity significantly suppresses the number of TB4 activated Tbx-18 and Wt-1 positive myocardial progenitor cells in the non infarcted remote areas (n=6). Bars indicate standard deviation at 95% confidence limits. *p < 0.05. ec, epicardium