[Retinoic acid induced cell cycle arrest and apoptosis in mouse embryonic palatal mesenchymal cells].
OBJECTIVE
To investigate the effect of all-trans retinoic acid (atRA) on proliferation activity and cell cycle distribution in mouse embryonic palatal mesenchymal (MEPM) cells and the underlying molecular mechanisms.


METHODS
MEPM cells were prepared from palate shelves of mouse fetal on gestation day 13. Cell viability was determined by MTI assay. Cell cycle distribution and subdiploid population were analyzed by cytometry. The expression of cyclin D and E and phosphorylation of retinoblastoma protein was examined using Western-blot.


RESULTS
atRA remarkably inhibited the growth of MEPM cells in a dose-dependent manner. atRA also caused an increase in the proportion of cells in G0/G1 and a decrease in the proportion of cells in S phase. atRA inhibited expression of cyclins D and E at protein level. Furthermore, atRA treatment reduced phosphorylated Rb.


CONCLUSIONS
These data suggested that atRA had antiproliferative activity by modulating G1/S cell cycle regulators and by inhibition of Rb phosphorylation in MEPM cells, which might account for the pathogenesis of cleft palate induced by retinoic acid.
Yu
Zeng-Li
ZL
Stomatology Hospital, Peking University, Beijing 100018, China.
Lin
Jiu-Xiang
JX
Xiao
Ying
Y
Han
Jing
J
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects*; D002478:Cells, Cultured; D002972:Cleft Palate / Q000139:chemically induced; D004622:Embryo, Mammalian; D005260:Female; D008648:Mesoderm / Q000166:cytology / Q000187:drug effects*; D051379:Mice; D010159:Palate / Q000166:cytology / Q000187:drug effects* / Q000196:embryology; D016160:Retinoblastoma Protein / Q000378:metabolism; D013723:Teratogens / Q000633:toxicity; D014212:Tretinoin / Q000633:toxicity*
D016160:Retinoblastoma Protein; D013723:Teratogens; D014212:Tretinoin