P38介导Wnt6促人牙乳头细胞分化的作用机制
P38介导Wnt6促人牙乳头细胞分化的作用机制
【目的】研究p38 MAPK通路在Wnt6促人牙乳头细胞分化中的作用机制。【方法】构建PGK-Wnt6过表达慢病毒;通过感染人牙乳头细胞(human dental papilla cells,HDPCs)过表达Wnt6蛋白;采用CCK-8和Annexin V-FITC双染法检测过表达Wnt6对HDPCs增殖、凋亡的影响;通过Western blot检测过表达Wnt6对p38通路的作用; 采用 SB203580抑制p38通路后,通过ALP、茜素红染色及qPCR检测矿化相关基因,检测抑制p38后对过表达Wnt6促进HDPCs分化的影响。【结果】成功构建HDPCs过表达Wnt6模型;Wnt6过表达对HDPCs的增殖、凋亡无明显作用;Western blot证实Wnt6上调p38的磷酸化水平;茜素红、ALP染色发现SB203580显著抑制过表达Wnt6所致的HDPCs的矿化,同时qPCR检测发现早期矿化基因ALP、COL I的表达被显著抑制,但矿化晚期基因DSPP、OC无明显变化。【结论】p38MAPK通路介导了Wnt6促HDPCs分化的早期过程。
Objective: to study the effect of p38 on the differentiation promoted by Wnt6 in HDPCs. Methods: PGK-Wnt6 overexpression lentivirus was constructed; infected HDPCs with Wnt6 lentivirus overexpressed Wnt6; the proliferation and apoptosis of HDPCs influenced by Wnt6 virus were not changed obviously; the phosphorylation of p38 activated by Wnt6 was determined by Western blot; Alizarin red, ALP staining and qPCR were used to verify whether SB203580, a p38 inhibitor, can block the differentiation of HDPCs promoted by Wnt6. Results: The Wnt6 overexpression model in HDPCs was established; there were no obvious changes of HDPCs proliferation after infected with PGK-Wnt6 lentivirus; SB203580 treatment significantly reduced increased mineralization and the expression of osteogenic genes, including ALP and Col I, which were induced by Wnt6, but OC and DSPP have no significant changes. Conclusion:p38 mediates the early differentiation of HDPCs promoted by Wnt6.
杨静、汪成林、宋天柱、叶玲
基础医学口腔科学
口腔基础医学Wnt6p38人牙乳头细胞
Basic Science of StomatologyWnt6p38human dental papilla cell
杨静,汪成林,宋天柱,叶玲.P38介导Wnt6促人牙乳头细胞分化的作用机制[EB/OL].(2016-05-24)[2025-08-16].http://www.paper.edu.cn/releasepaper/content/201605-1016.点此复制
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