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Updated: Aug 14, 2026
Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
Published on: April 22, 2017
[Retinoic acid induced cell cycle arrest and apoptosis in mouse embryonic palatal mesenchymal cells]
Zeng-Li Yu1, Jiu-Xiang Lin, Ying Xiao
1Stomatology Hospital, Peking University, Beijing 100018, China.
Objectives:
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.
Conclusion:
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.
Insights
All-trans retinoic acid (atRA) inhibits mouse embryonic palatal mesenchymal cell proliferation by affecting cell cycle regulators and retinoblastoma protein phosphorylation. This provides insight into retinoic acid-induced cleft palate pathogenesis.
Area of Science:
- Developmental Biology
- Molecular Biology
- Cell Biology
Context:
- Retinoic acid signaling plays a critical role in embryonic development, including palate formation.
- Aberrant retinoic acid levels are implicated in teratogenesis, such as cleft palate.
- Understanding the cellular mechanisms of retinoic acid action is crucial for developmental toxicology.
Purpose:
- To elucidate the impact of all-trans retinoic acid (atRA) on mouse embryonic palatal mesenchymal (MEPM) cell proliferation.
- To investigate the effects of atRA on MEPM cell cycle distribution and key regulatory proteins.
- To explore the molecular mechanisms underlying atRA's influence on MEPM cells.
Summary:
- All-trans retinoic acid (atRA) significantly inhibited MEPM cell viability in a dose-dependent manner.
- atRA treatment led to cell cycle arrest at the G0/G1 phase and reduced S phase population.
- atRA suppressed the protein expression of cyclins D and E and decreased retinoblastoma protein (Rb) phosphorylation.
Impact:
- The findings demonstrate that atRA exhibits antiproliferative effects on MEPM cells.
- atRA modulates G1/S cell cycle transition regulators and inhibits Rb phosphorylation.
- These cellular effects may contribute to the pathogenesis of retinoic acid-induced cleft palate.
