Effects of calponin-1 gene silencing on the biological behavior of uterine smooth muscle cells.
- Author:
Yong-hong GU
1
;
Chang-ju ZHOU
;
Lin-yu HU
;
Qian CHEN
;
Wei-she ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Calcium-Binding Proteins; genetics; Cell Movement; Cell Proliferation; Cells, Cultured; Female; Gene Silencing; Humans; Microfilament Proteins; genetics; Myocytes, Smooth Muscle; cytology; metabolism; RNA Interference; RNA, Small Interfering; genetics; Uterus; cytology; metabolism
- From: Journal of Southern Medical University 2010;30(6):1369-1372
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of calponin-1 expression inhibition on the proliferation , invasiveness, apoptosis and cytoskeleton of uterine smooth muscle cells, and explore the molecular mechanism of calponin-1 in the uterine smooth muscle cells for labor onset.
METHODSsiRNA-calponin-1 adenovirus plasmid was constructed and transfected into primarily cultured uterine smooth muscle cells. The proliferation, invasiveness and apoptosis of the cells were determined by MTT assay, matrigel invasion assays and flow cytometry, respectively. Rhodamine-Phalloidin was used for labeling filamentous actin (F-actin), and the morphology and the distribution of F-actin was observed under fluorescence microscopy and analyzed quantitatively.
RESULTSThe motor ability of uterine smooth muscle cells decreased significantly after transfection with siRNA-calponin-1 adenovirus plasmid (P<0.05). The transfected cells showed thinner, loosened and irregular F-actin microfibers, and the cells in the empty vector and blank control groups showed thicker and longer F-actin microfibers.
CONCLUSIONInhibition of calponin-1 expression can inhibit uterine smooth muscle cell migration and cause the morphological change and rearrangement of F-actin without affecting its proliferation and apoptosis in vitro, suggesting that the morphological change and rearrangement of F-actin of uterine smooth muscle cell may be one of the important mechanisms in the labor onset.