WD Repeat Domain 1 Deficiency Inhibits Neointima Formation in Mice Carotid Artery by Modulation of Smooth Muscle Cell Migration and Proliferation.

The migration, dedifferentiation, and proliferation of vascular smooth muscle cells (VSMCs) are responsible for intimal hyperplasia, but the mechanism of this process has not been elucidated. WD repeat domain 1 (WDR1) promotes actin-depolymerizing factor (ADF)/cofilin-mediated depolymerization of actin filaments (F-actin). The role of WDR1 in neointima formation and progression is still unknown.

[The role of actin cytoskeleton in regulating the deployment process of mouse cardiac second heart field progenitor cells].

The vertebrate heart tube originates from cardiogenic mesodermal cells in the early embryo, and subsequently elongates by progressive addition of second heart field (SHF) progenitor cells from adjacent pharyngeal mesoderm and splanchnic mesoderm. Insufficient addition of SHF cells to the heart tube causes the failure of maximal elongation of the heart tube, which results in a series of developmental defects including the most common congenital birth defects, such as right ventricular dysplasia and outflow tract septation, and alignment anomalies. SHF cells form an atypical, apicobasally polarized epithelium which is characterized by apical monocilia, and dynamic actin-rich basal filopodia.

ERα inhibited myocardin-induced differentiation in uterine fibroids.

Uterine fibroids, also known as uterine leiomyomas, are a benign tumor of the human uterus and the commonest estrogen-dependent benign tumor found in women. Myocardin is an important transcriptional regulator in smooth and cardiac muscle development. The role of myocardin and its relationship with ERα in uterine fibroids have barely been addressed.