Microtia patients: Auricular chondrocyte ECM is promoted by CGF through IGF-1 activation of the IGF-1R/PI3K/AKT pathway

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  • 作者:Xia Chen, Ruhong Zhang, Qun Zhang, Zhicheng Xu, Feng Xu, Datao Li, Yiyuan Li
  • 期刊:JOURNAL OF CELLULAR PHYSIOLOGY
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Objective:To explore the effectiveness of the insulin-like growth factor 1 receptor (IGF-1R)/PI3K/AKT pathway in promoting the synthesis of the auricular chondrocyte extracellular matrix (ECM) using concentrated growth factor (CGF).

Methods:Chondrocytes isolated from the remnant auricular cartilage of microtia patients were randomly divided into different experimental and control groups, then stimulated with a reagent. IGF-1 released by CGF was quantified by enzyme-linked immunosorbent assay. Glycosaminoglycan (GAG), proteoglycan, and type II collagen (COLAII) were examined by histological and immunohistological analysis. Expression levels of IGF-1R, pIGF-1R, PI3K, pPI3K, AKT, pAKT, COLAII, and Aggrecan were detected by western blot analysis technique and gene expression was tested by real-time polymerase chain reaction.

Results:CGF significantly stimulated the synthesis of COLAII and Aggrecan and increased the phosphorylation levels of IGF-1R, PI3K, and AKT. Small interfering RNA IGF-1 blocked ECM synthesis, COLAII and Aggrecan gene expression, and IGF-1R/PI3K/AKT activation. Inhibitor AG1024 and LY294002 significantly inhibited ECM synthesis and the phosphorylation of IGF-1R, PI3K, and AKT.

Conclusion:CGF-released IGF-1 stimulates the synthesis of the auricular chondrocyte ECM via the IGF-1R/PI3K/AKT signaling pathway.

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