Li Jieli, Liu Yang, Jin Yixin, Wang Rui, Wang Jian, Lu Sarah, VanBuren Vincent, Dostal David E, Zhang Shenyuan L, Peng Xu
Department of Medical Physiology, College of Medicine, Texas A&M University, USA.
Department of Medical Physiology, College of Medicine, Texas A&M University, USA; Department of Cardiology, Yangpu District Central Hospital, Tongji University, China.
Dev Biol. 2017 Jan 15;421(2):271-283. doi: 10.1016/j.ydbio.2016.12.012. Epub 2016 Dec 14.
Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cell migration, proliferation, differentiation and survival. However, the role of Cdc42 in heart development remains largely unknown. To determine the function of Cdc42 in heart formation, we have generated a Cdc42 cardiomyocyte knockout (CCKO) mouse line by crossing Cdc42 flox mice with myosin light chain (MLC) 2a-Cre mice. The inactivation of Cdc42 in embryonic cardiomyocytes induced lethality after embryonic day 12.5. Histological analysis of CCKO embryos showed cardiac developmental defects that included thin ventricular walls and ventricular septum defects. Microarray and real-time PCR data also revealed that the expression level of p21 was significantly increased and cyclin B1 was dramatically decreased, suggesting that Cdc42 is required for cardiomyocyte proliferation. Phosphorylated Histone H3 staining confirmed that the inactivation of Cdc42 inhibited cardiomyocytes proliferation. In addition, transmission electron microscope studies showed disorganized sarcomere structure and disruption of cell-cell contact among cardiomyocytes in CCKO hearts. Accordingly, we found that the distribution of N-cadherin/β-Catenin in CCKO cardiomyocytes was impaired. Taken together, our data indicate that Cdc42 is essential for cardiomyocyte proliferation, sarcomere organization and cell-cell adhesion during heart development.
Cdc42是Rho GTPase家族的成员,作为分子开关参与调节细胞迁移、增殖、分化和存活。然而,Cdc42在心脏发育中的作用仍 largely未知。为了确定Cdc42在心脏形成中的功能,我们通过将Cdc42 flox小鼠与肌球蛋白轻链(MLC)2a-Cre小鼠杂交,构建了Cdc42心肌细胞敲除(CCKO)小鼠品系。胚胎心肌细胞中Cdc42的失活在胚胎第12.5天后导致死亡。对CCKO胚胎的组织学分析显示心脏发育缺陷,包括心室壁变薄和室间隔缺损。微阵列和实时PCR数据还显示p21的表达水平显著增加,细胞周期蛋白B1显著降低,这表明Cdc42是心肌细胞增殖所必需的。磷酸化组蛋白H3染色证实Cdc42的失活抑制了心肌细胞增殖。此外,透射电子显微镜研究显示CCKO心脏中心肌细胞的肌节结构紊乱,细胞间接触破坏。因此,我们发现CCKO心肌细胞中N-钙黏蛋白/β-连环蛋白的分布受损。综上所述,我们的数据表明Cdc42在心脏发育过程中对心肌细胞增殖、肌节组织和细胞间黏附至关重要。