scholarly journals Netrin-1 regulates the inflammatory response of neutrophils and macrophages, and suppresses ischemic acute kidney injury by inhibiting COX-2-mediated PGE2 production

2013 ◽  
Vol 83 (6) ◽  
pp. 1087-1098 ◽  
Author(s):  
Punithavathi V. Ranganathan ◽  
Calpurnia Jayakumar ◽  
Riyaz Mohamed ◽  
Zheng Dong ◽  
Ganesan Ramesh
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Response ◽  
Kidney Injury ◽  
Pge2 Production ◽  
Ischemic Acute Kidney Injury ◽  
Cox 2

scholarly journals Impact of steroids on the inflammatory response after ischemic acute kidney injury in rats

2017 ◽  
Vol 27 (5) ◽  
pp. 365 ◽  
Author(s):  
J Fontana ◽  
A Vogt ◽  
A Hohenstein ◽  
U Vettermann ◽  
E Doroshenko ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Response ◽  
Kidney Injury ◽  
Ischemic Acute Kidney Injury

scholarly journals Negative Regulation of TGFβ Signaling by Stem Cell Antigen-1 Protects against Ischemic Acute Kidney Injury

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0129561 ◽  
Author(s):  
Troy D. Camarata ◽  
Grant C. Weaver ◽  
Alexandr Vasilyev ◽  
M. Amin Arnaout
Keyword(s):  
Acute Kidney Injury ◽  
Stem Cell ◽  
Kidney Injury ◽  
Negative Regulation ◽  
Tgfβ Signaling ◽  
Cell Antigen ◽  
Ischemic Acute Kidney Injury

scholarly journals MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xudong Wang ◽  
Yali Wang ◽  
Mingjian Kong ◽  
Jianping Yang
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Response ◽  
Periodic Acid ◽  
Kidney Injury ◽  
Luciferase Reporter ◽  
Tunel Staining ◽  
Tnf Α

Abstract Background: Septic acute kidney injury is considered as a severe and frequent complication that occurs during sepsis. The present study was performed to understand the role of miR-22-3p and its underlying mechanism in sepsis-induced acute kidney injury. Methods: Rats were injected with adenovirus carrying miR-22-3p or miR-NC in the caudal vein before cecal ligation. Meanwhile, HK-2 cells were transfected with the above adenovirus following LPS stimulation. We measured the markers of renal injury (blood urea nitrogen (BUN), serum creatinine (SCR)). Histological changes in kidney tissues were examined by hematoxylin and eosin (H&E), Masson staining, periodic acid Schiff staining and TUNEL staining. The levels of IL-1β, IL-6, TNF-α and NO were determined by ELISA assay. Using TargetScan prediction and luciferase reporter assay, we predicted and validated the association between PTEN and miR-22-3p. Results: Our data showed that miR-22-3p was significantly down-regulated in a rat model of sepsis-induced acute kidney injury, in vivo and LPS-induced sepsis model in HK-2 cells, in vitro. Overexpression of miR-22-3p remarkably suppressed the inflammatory response and apoptosis via down-regulating HMGB1, p-p65, TLR4 and pro-inflammatory factors (IL-1β, IL-6, TNF-α and NO), both in vivo and in vitro. Moreover, PTEN was identified as a target of miR-22-3p. Furthermore, PTEN knockdown augmented, while overexpression reversed the suppressive role of miR-22-3p in LPS-induced inflammatory response. Conclusions: Our results showed that miR-22-3p induced protective role in sepsis-induced acute kidney injury may rely on the repression of PTEN.

Ischemic acute kidney injury and klotho in renal transplantation

2018 ◽  
Vol 55 ◽  
pp. 3-8 ◽  
Author(s):  
Fatemeh Panah ◽  
Amir Ghorbanihaghjo ◽  
Hassan Argani ◽  
Maryam Asadi Zarmehri ◽  
Saeed Nazari Soltan Ahmad
Keyword(s):  
Acute Kidney Injury ◽  
Renal Transplantation ◽  
Kidney Injury ◽  
Ischemic Acute Kidney Injury
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