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Sox9 Protects against Human Lung Fibroblast Cell Apoptosis Induced by LPS through Activation of the AKT/GSK3β Pathway

Zhankun Zhu1, Jinhua Dai1, Yufeng Liao1, and Tao Wang2*

1Ningbo No. 2 Hospital, Department of Clinical Laboratory, 315010 Ningbo, Zhejiang, China

2First Affiliated Hospital of Xiamen University, Department of Clinical Laboratory, 361003 Xiamen, Fujian, China; E-mail: wangtao9596@126.com

* To whom correspondence should be addressed.

Received September 9, 2016; Revision received October 25, 2016
Sex-determining region Y-box 9 (Sox9) is an important transcription factor that has been identified as a key regulator of several types of diseases. In this study, we explored the correlation of Sox9 with cell proliferation, apoptosis, inflammatory factor expression, and the possible signaling pathway in human lung fibroblast cell line to investigate the possible mechanism of neonatal pneumonia. Therefore, in the present study, pc-Sox9 and si-Sox9 were transfected into MRC-5 (human fetal lung fibroblast cell line) to promote or inhibit expression of Sox-9. Quantitative reverse-transcription polymerase chain reaction and Western blot were used to determine the expression level of Sox-9 at mRNA and protein level. Then 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry were used to explore, respectively, proliferation and apoptosis in vitro. We found that Sox9 could significantly upregulate the proliferation rate and inhibit apoptosis rate and inflammatory factor expression of MRC-5 cells compared with a control group. Moreover, the signaling pathway study confirmed that Sox9 protected MRC-5 from lipopolysaccharide injury through the AKT/GSK3β pathway. All these findings suggest that Sox9 acts as a novel marker for neonatal pneumonia and could be a new therapeutic target for this disease.
KEY WORDS: Sox9, neonatal pneumonia, MRC-5, LPS, cell apoptosis

DOI: 10.1134/S000629791705008X