胚胎心肌细胞中Cdc42的缺失导致右心室发育不全。
Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia.
作者信息
Liu Yang, Wang Jian, Li Jieli, Wang Rui, Tharakan Binu, Zhang Shenyuan L, Tong Carl W, Peng Xu
机构信息
Department of Medical Physiology, College of Medicine, Texas A&M University, Temple, USA.
Department of Obstetrics and Gynecology, Baylor Scott & White Health, Temple, USA.
出版信息
Clin Transl Med. 2017 Nov 3;6(1):40. doi: 10.1186/s40169-017-0171-4.
BACKGROUND
Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cytoskeleton remodeling and cell polarity establishment. Inactivating Cdc42 in cardiomyocytes resulted in embryonic lethality with heart developmental defects, including ventricular septum defects and thin ventricle wall syndrome.
FINDINGS
In this study, we have generated a Cdc42 cardiomyocyte knockout mouse line by crossing Cdc42/flox mice with myosin light chain 2a (MLC2a)-Cre mice. We found that the deletion of Cdc42 in embryonic cardiomyocytes resulted in an underdeveloped right ventricle. Microarray analysis and real-time PCR data analysis displayed that the deletion of Cdc42 decreased dHand expression level. In addition, we found evaginations in the ventricle walls of Cdc42 knockout hearts.
CONCLUSION
We concluded that Cdc42 plays an essential role in right ventricle growth.
背景
Cdc42是Rho GTPase家族的成员，作为分子开关调节细胞骨架重塑和细胞极性建立。在心肌细胞中使Cdc42失活会导致胚胎致死，并伴有心脏发育缺陷，包括室间隔缺损和心室壁变薄综合征。
研究结果
在本研究中，我们通过将Cdc42/flox小鼠与肌球蛋白轻链2a（MLC2a）-Cre小鼠杂交，构建了Cdc42心肌细胞敲除小鼠品系。我们发现胚胎心肌细胞中Cdc42的缺失导致右心室发育不全。微阵列分析和实时PCR数据分析显示，Cdc42的缺失降低了dHand的表达水平。此外，我们在Cdc42敲除心脏的心室壁中发现了内陷。
结论
我们得出结论，Cdc42在右心室生长中起重要作用。
Zotero 插件