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Figure 3 | BMC Physiology

Figure 3

From: Forced expression of the cell cycle inhibitor p57Kip2 in cardiomyocytes attenuates ischemia-reperfusion injury in the mouse heart

Figure 3

Forced p57Kip 2expression in the embryonic heart does not impair cardiomyocyte proliferation. Localization of p57Kip2 and Ki-67 in ventricular cardiomyocytes of E9.5 wild type (WT) and R26loxpTA-p57k/+;Mlc2v-Crek/+animals by indirect immunofluorescence. In WT E9.5 cardiomyocytes p57Kip2 is not yet expressed (A-C). However, p57Kip2 is expressed in most cardiomyocytes of the R26loxpTA-p57k/+;Mlc2v-Cre+/- mouse embryos as early as E9.5 (D-F). Expression of p57Kip2 in embryonic cardiomyocytes does not preclude Ki-67 expression (E, F). DNA synthesis in the heart of R26loxpTA-p57k/+;Mlc2v-Crek/+transgenic mice is similar to the hearts of wild type animals despite the abundance of p57Kip2 protein in the cardiomyocytes of the transgenic hearts. In the merged pictures (third column), the yellow nuclei represent cardiomyocytes co-labeled by both antibodies. High power magnification of the same cardiomyocyte labeled with both antibodies, illustrates that although there are many cells stained with both p57Kip2 and Ki-67, in most cells p57Kip2 and Ki-67 immunoreactivity occur in exclusive nuclear domains (G, H, I).

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