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p38和Erk1/2对牙髓干细胞软骨生成和成骨分化的不同影响。

Differential effects of p38 and Erk1/2 on the chondrogenic and osteogenic differentiation of dental pulp stem cells.

作者信息

Ba Pengfei, Duan Xiaoyu, Fu Guo, Lv Shuyan, Yang Pishan, Sun Qinfeng

机构信息

Department of Periodontology, School of Stomatology, Shandong University, Jinan, Shandong 250012, P.R. China.

National Engineering Laboratory, WeGo Group Co., Ltd., Weihai, Shandong 264210, P.R. China.

出版信息

Mol Med Rep. 2017 Jul;16(1):63-68. doi: 10.3892/mmr.2017.6563. Epub 2017 May 10.

DOI:10.3892/mmr.2017.6563
PMID:28498451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5482129/
Abstract

The extracellular signal-regulated protein kinase 1/2 (Erk1/2) and p38 mitogen‑activated protein‑kinase pathways serve important roles in the regulation of osteogenic and chondrogenic differentiation in mesenchymal stem cells (MSCs). However, the exact mechanism remains unclear, and the effect is controversial. In the present study, the effects of Erk1/2 and p38 on the osteogenic and chondrogenic differentiation of dental pulp stem cells (DPSCs) were compared in vitro. The results indicated that inhibition of Erk1/2 is able to enhance the osteogenic differentiation of DPSCs and inhibit chondrogenic differentiation, whereas inhibition of p38 demonstrated the opposite effect. When compared with previous studies, the present study further confirmed that Erk1/2 and p38 serve important, but complicated, roles in regulating the differentiation of MSCs. Different chemical and physical stimuli, cell types, culture methods, times of inhibitor administration and the dosage of the inhibitor may influence the effect of Erk1/2 and p38 on the differentiation of MSCs. The present study aims to better understand the mechanisms that control the differentiation of MSCs and may be helpful in creating more effective tissue regeneration.

摘要

细胞外信号调节蛋白激酶1/2(Erk1/2)和p38丝裂原活化蛋白激酶信号通路在间充质干细胞(MSC)成骨和成软骨分化的调控中发挥重要作用。然而,确切机制仍不清楚,且其作用存在争议。在本研究中,体外比较了Erk1/2和p38对牙髓干细胞(DPSC)成骨和成软骨分化的影响。结果表明,抑制Erk1/2能够增强DPSC的成骨分化并抑制软骨分化,而抑制p38则表现出相反的效果。与先前的研究相比,本研究进一步证实Erk1/2和p38在调控MSC分化中发挥重要但复杂的作用。不同的化学和物理刺激、细胞类型、培养方法、抑制剂给药时间以及抑制剂剂量可能会影响Erk1/2和p38对MSC分化的作用。本研究旨在更好地理解控制MSC分化的机制,并可能有助于实现更有效的组织再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/21b7e1a3be11/MMR-16-01-0063-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/d598de6f5702/MMR-16-01-0063-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/01db615eaa20/MMR-16-01-0063-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/21b7e1a3be11/MMR-16-01-0063-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/d598de6f5702/MMR-16-01-0063-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/01db615eaa20/MMR-16-01-0063-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db5/5482129/21b7e1a3be11/MMR-16-01-0063-g02.jpg

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