【Background】
Mammalian cardiomyocytes (CMs) retain proliferative capacity shortly after birth, though these cells are differentiated with contractile activity. By using Runx1 as a dedifferentiation marker, recent studies have demonstrated that CMs are dedifferentiated prior to cell proliferation; however, biological significance of Runx1 remains to be fully elucidated. The aim of this research is to clarify the regulatory mechanisms of Runx1 expression and its biological functions in CM proliferation.
【Method/Result】
CMs were prepared from neonatal rats. Cell proliferative activity was estimated by immune-fluorescent microscopic analysis with anti-Ki-67 antibody. CM exhibited proliferative activity in response to fetal bovine serum (FBS). Previously, since we demonstrated that STAT3 plays an important role in CM proliferation, the effects of STAT3 on CM proliferation was analyzed by using siRNA. STAT3 knockdown reduced the frequency of Ki-67⁺ CM, accompanied by the decrease in Runx1 expression. Importantly, Runx1 knockdown also suppressed CM proliferation in response to FBS.
【Conclusion】
Runx1 expression is regulated by STAT3, and promotes CM proliferation, indicating the functional importance of Runx1 in cardiac proliferation.