Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway
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Lili Shen1,2, Tiancheng Zhang3,4 and Hongyan Lu1
1Department of Pediatrics, The Affiliated Hospital of Jiangsu University, Zhenjiang, China
2Department of Pediatrics, Suzhou Kowloon Hospital Shanghai Jiao Tong University School of Medicine, Suzhou, China
3Institute of Reproduction and Development, Fudan University, Shanghai, China
4China National Population and Family Planning Key Laboratory of Contraceptive Drugs and Devices, Shanghai Institute of Planned Parenthood Research (SIPPR), Shanghai, China
Hongyan Lu, email: firstname.lastname@example.org
Keywords: differentially expressed gene; functional enrichment analysis; broncopulmonary dysplasia; angiotensinogen; inflammation
Received: May 13, 2017 Accepted: July 25, 2017 Published: October 10, 2017
Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. The present study aimed to investigate the roles of the AGT in the progression of broncopulmonary dysplasia in premature newborns. By bioinformatics analysis, AGT was found to be the major node in molecular interaction networks of BPD mouse model. Quantitative PCR and western blot analyses were applied to examine AGT expression in A549 cells which were treated with the hyperoxic condition. The AGT inhibitor Valsartan and the AGT agonist ANGII were employed to investigate the roles of AGT in cell growth and the inflammation. Results show that hyperoxic treatment induced upregulation of AGT expression in A549 cells. Overexpression of AGT resulted in the inflammation via the JAK/STAT signal pathway, ultimately suppressed the proliferation of the A549 cell. In conclusion, increased expression of AGT was demonstrated to be associated with the development and progression of BPD, and may be regarded as a promising therapeutic target for BPD.
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