Deregulation of long noncoding RNA (TUG1) contributes to excessive podocytes apoptosis by activating endoplasmic reticulum stress in the development of diabetic nephropathy

• Published in: Journal of cellular physiology Vol. 234; no. 9; pp. 15123 - 15133
• Main Authors: Shen, Hongchun, Ming, Yao, Xu, Chuanlan, Xu, Yanwen, Zhao, Sha, Zhang, Qiong
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.09.2019
• Subjects: Apoptosis; Caspase; CCAAT/enhancer-binding protein; CHOP; CHOP protein; Deregulation; Diabetes; Diabetes mellitus; Diabetic nephropathy; DNA nucleotidylexotransferase; Endoplasmic reticulum; endoplasmic reticulum stress; Glucose; Homology; Nephropathy; podocytes, PGC‐1α; Polymerase chain reaction; Proteins; Signal transduction; siRNA; TUG1; CHOP; apoptosis; TUG1; podocytes, PGC-1α; diabetic nephropathy; endoplasmic reticulum stress

The objective of this study was to investigate the molecular mechanism of how TUG1 interferes with the expression of C/EBP homologous protein (CHOP), peroxisome‐proliferator‐activated receptor‐γ coactivator‐1 alpha (PGC‐1α), which contributes to the development of diabetic nephropathy. Real‐time pol...