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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Am+Soc+Nephrol
2016 ; 27
(3
): 863-76
Nephropedia Template TP
gab.com Text
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English Wikipedia
Angiogenin Mediates Cell-Autonomous Translational Control under Endoplasmic
Reticulum Stress and Attenuates Kidney Injury
#MMPMID26195817
Mami I
; Bouvier N
; El Karoui K
; Gallazzini M
; Rabant M
; Laurent-Puig P
; Li S
; Tharaux PL
; Beaune P
; Thervet E
; Chevet E
; Hu GF
; Pallet N
J Am Soc Nephrol
2016[Mar]; 27
(3
): 863-76
PMID26195817
show ga
Endoplasmic reticulum (ER) stress is involved in the pathophysiology of kidney
disease and aging, but the molecular bases underlying the biologic outcomes on
the evolution of renal disease remain mostly unknown. Angiogenin (ANG) is a
ribonuclease that promotes cellular adaptation under stress but its contribution
to ER stress signaling remains elusive. In this study, we investigated the
ANG-mediated contribution to the signaling and biologic outcomes of ER stress in
kidney injury. ANG expression was significantly higher in samples from injured
human kidneys than in samples from normal human kidneys, and in mouse and rat
kidneys, ANG expression was specifically induced under ER stress. In human renal
epithelial cells, ER stress induced ANG expression in a manner dependent on the
activity of transcription factor XBP1, and ANG promoted cellular adaptation to ER
stress through induction of stress granules and inhibition of translation.
Moreover, the severity of renal lesions induced by ER stress was dramatically
greater in ANG knockout mice (Ang(-/-)) mice than in wild-type mice. These
results indicate that ANG is a critical mediator of tissue adaptation to kidney
injury and reveal a physiologically relevant ER stress-mediated adaptive
translational control mechanism.