Long non-coding RNA PlncRNA-1 regulates cell proliferation, apoptosis, and autophagy in septic acute kidney injury by regulating BCL2.

Abstract

This study aimed to elucidate the potential role of long non-coding RNA PlncRNA-1 in the septic acute kidney injury (AKI). The expression of PlncRNA-1 in the serum of patients with septic AKI patient was detected. We then established lipopolysaccharide (LPS)-induced septic AKI model in NRK-52E cells to investigate the effects of the overexpression of PlncRNA-1 on cell proliferation, apoptosis, and autophagy. In addition, the regulatory relationship between PlncRNA-1 and B-cell lymphoma 2 (BCL2) was explored to further elucidate the regulatory mechanism of PlncRNA-1 in septic AKI. PlncRNA-1 is downregulated in the serum of patients with septic AKI and in LPS-induced septic AKI cells. The overexpression of PlncRNA-1 considerably increases proliferation and inhibits apoptosis and autophagy of LPS-induced septic AKI cells. In addition, PlncRNA-1 can promote BCL2 expression, and the overexpression of BCL2 enhances proliferation and inhibits apoptosis and autophagy of LPS-induced septic AKI cells. Our findings reveal that the overexpression of PlncRNA-1 may promote cell proliferation and inhibit apoptosis and autophagy in septic AKI by regulating BCL2 expression. PlncRNA-1 may serve as a potential biomarker or target for the diagnosis and treatment of septic AKI.

• Authors: Dian Fu, Kai Zhou, Jun Liu, Peng Zheng, Ping Li, Wen Cheng, Zhenyu Xu, Jingping Ge, Zhengyu Zhang, Wenquan Zhou, Jie Dong
• Journal: International journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 11 Issue 1 Pg. 314-323 ( 2018) ISSN: 1936-2625 [Electronic] United States
• PMID: 31938114 (Publication Type: Journal Article)
• Copyright: IJCEP Copyright © 2018.