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Updated: Sep 20, 2026

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
Published on: February 13, 2021
[Study on the expression level of Annexin I, cPLA(2) and PCNA in cleft-palate mice induced by dexamethasone]
1Department of Oral and Maxillofacial Surgery, West China School of Stomatology, Sichuan University, Chengdu 610041, China.
Objective:
To test the changing expression level of Annexin I, cPLA(2) and PCNA in the palatine process of cleft-palate mice A/J and C57B/6j induced by dexamethasone. To discuss the developing mechanism of cleft-palate and the corresponding preventive methods.
Method:
s Pregnant mice A/J and C57BL/6j were randomly divided into normal group as blank control, group with deformity induced by dexamethasone, group given VitB(12) as antagonist to deforming factor, group given only VitB(12). The relative quantity of Annexin I, Cpla2 and PCNA were detected by immunoblotting.
Results:
Among mice A/J, with the development of palatine process, Annexin I's expression level was increased in the normal group, and other groups showed the similar changes. Annexin I's expression level was significantly higher in group DEX and group DEX + VitB(12) than in normal group and VitB(12) group of, while there was no significant difference between normal group and VitB(12) group. But the changes of cPLA(2) and PCNA expression level was in an opposite direction, with development it decreased in the normal mice's palatine process. In mice C57B/6j there was no significant difference between normal group and group DEX on the measured quantity of Annexin I, cPLA(2) and
Conclusions:
Annexin I and cPLA(2) introduce glucocorticoid to induce cleft-palate. VitB(12) can not inhibit DEX's enhancing effect on the expression level of Annexin I, but it can antagonize DEX's inhibiting effect on expression level of cPLA(2), which is probably one of the mechanisms why VitB(12) antagonize glucocorticoid's deforming effect.

