RRC ID 49243
Author Qin C, Xiao C, Su Y, Zheng H, Xu T, Lu J, Luo P, Zhang J.
Title Tisp40 deficiency attenuates renal ischemia reperfusion injury induced apoptosis of tubular epithelial cells.
Journal Exp Cell Res
Abstract Renal ischemia reperfusion (IR) is a major cause of acute kidney injury (AKI) and no effective treatments have been established. Tisp40 is a transcription factor of the CREB/ATF family and involves in cell apoptosis, proliferation and differentiation, but its role in renal IR remains unknown. Here, we investigated the role of Tisp40 in renal IR injury. In vivo, Tisp40 knockout (KO) and wild-type (WT) mice were subjected to thirty minutes of bilateral renal ischemia and 48h reperfusion, the blood and kidneys were harvested for analysis. In vitro, Tisp40 overexpression and vector cells were subjected to hypoxia/reoxygenation (HR), the apoptosis rate and the expressions of related proteins were measured. Following IR, the expressions of Tisp40 protein, serum creatinine (sCr), blood urea nitrogen (BUN) and apoptosis of tubular cells were significantly increased in WT mice. However, Tisp40 deficiency significantly attenuated the increase of sCr, BUN and apoptosis of tubular cells. Following HR, apoptosis of tubular cells was increased in Tisp40 overexpression cells compared with vector cells. Mechanistically, Tisp40 promoted the expressions of C/EBP homologous protein (CHOP), Bax and Cleaved caspase3 and suppressed the expression of Bcl-2 in renal IR injury. In conclusion, Tisp40 aggravates tubular cells apoptosis in renal IR injury.
Volume 359(1)
Pages 138-144
Published 2017-10-1
DOI 10.1016/j.yexcr.2017.07.038
PII S0014-4827(17)30409-3
PMID 28778797
MeSH Animals Apoptosis* Cyclic AMP Response Element-Binding Protein / deficiency* Cyclic AMP Response Element-Binding Protein / metabolism Epithelial Cells / metabolism* Epithelial Cells / pathology Hypoxia / complications Hypoxia / pathology Kidney Tubules / abnormalities Kidney Tubules / pathology* Kidney Tubules / physiopathology Mice, Inbred C57BL Mice, Knockout Oxygen Reperfusion Injury / metabolism* Reperfusion Injury / pathology* Reperfusion Injury / physiopathology Transcription Factor CHOP / metabolism
IF 3.383
Times Cited 5
Mice RBRC01942