Expression of PI3K/AKT Signaling Pathway in IFN-β-induced Differentiation of Human Mesenchymal Stem Cells into Chondroblasts

Expression of PI3K/AKT Signaling Pathway in IFN-β-induced Differentiation of Human Mesenchymal Stem Cells into Chondroblasts

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Author(s)

Author(s): Zhang Li-Jun, Huang Zhi-Li, Wang Yan, Li Qiao-Qiao

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DOI: 10.18483/ijSci.2156 36 137 23-28 Volume 8 - Aug 2019

Abstract

Induction of chondrogenic differentiation from MSCs are necessary for qualification as sources of seed cells for cartilage tissue engineering。Our previous research showed IFN-β maybe as a helper of TGF-βto promote chondrogenesis of hMSCs. In this paper, we investigated the expression of PI3K/AKT during the chondrogenic differentiation of hMSCs,hMSCs were divided into Blank control group, TGF-β3 group and TGF-β3+IFN-β1a group and then were induced into cartilage pellets respectively . At day 4,7,14,21, the pellets were collected and qRT-PCR and Western blotting were used to detect the relative expression of PI3K and AKT. The qPCR results showed that the mRNA expression levels of PI3K and AKT were up-regulated by TGF-β3 induced. Furthermore, the synergetic effect of TGF-β3 and IFN-β1a would up-regulate the mRNA expression levels of PI3K and AKT significantly. The Western blotting results showed that TGF-β3 also could up-regulate the expression of PI3K protein and with IFN-β1a the expression level increased significantly. However, according to AKT protein, TGF-β3 maybe only could up-regulate AKT(S473) expression, and with IFN-β1a the AKT(T308) expression could be up-regulated .These results showed that the synergetic effect of TGF-β3 and IFN-β1a could up-regulate the gene expression in PI3K/AKT signaling pathway and then promote hMSCs chondrogenic differentiation.

Keywords

PI3K/AKT Signaling Pathway, hMSCs, Chondrogenic Differentiation

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International Journal of Sciences is Open Access Journal.
This article is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.
Author(s) retain the copyrights of this article, though, publication rights are with Alkhaer Publications.

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