The effects of adenosine A2A receptor knockout on renal interstitial fibrosis in a mouse model of unilateral ureteral obstruction

2013 ◽  
Vol 115 (4) ◽  
pp. 315-319 ◽  
Author(s):  
Hang Xiao ◽  
Liang-Yi Si ◽  
Wei Liu ◽  
Nian Li ◽  
Gang Meng ◽  
...  
Keyword(s):  
Mouse Model ◽  
Ureteral Obstruction ◽  
Interstitial Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Adenosine A2a Receptor ◽  
Renal Interstitial Fibrosis ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Adenosine A2A Receptor: A Target for Regulating Renal Interstitial Fibrosis in Obstructive Nephropathy

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e60173 ◽  
Author(s):  
Hang Xiao ◽  
Hai-Ying Shen ◽  
Wei Liu ◽  
Ren-ping Xiong ◽  
Ping Li ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Adenosine A2a Receptor ◽  
Obstructive Nephropathy ◽  
Renal Interstitial Fibrosis ◽  
A2a Receptor ◽  
Adenosine A2a

Inhibition of CTCF-regulated miRNA-185-5p mitigates renal interstitial fibrosis of chronic kidney disease

Epigenomics ◽  
2021 ◽  
Author(s):  
Jiajun Zhou ◽  
Han Zhou ◽  
Yong Liu ◽  
Caixin Liu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mouse Model ◽  
Ureteral Obstruction ◽  
Interstitial Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Renal Interstitial Fibrosis ◽  
Underlying Mechanisms

Aim: The present study aimed to elucidate the effect of CTCF on renal interstitial fibrosis in chronic kidney disease (CKD) and underlying mechanisms. Materials & methods: We measured NPHS2 expression and investigated its function in a unilateral ureteral obstruction-induced mouse model of CKD. Results: NPHS2 was poorly expressed in CKD mice. miR-185-5p targeted NPHS2 and reduced its expression, leading to increased α-SMA and COL I/III expression, increased renal interstitial fibrosis area and elevated phosphorylated vasodilator-stimulated phosphoprotein/vasodilator-stimulated phosphoprotein ratio. Cotreatment with CTCF downregulated miR-185-5p expression and abolished its effects in the CKD model. Conclusion: CTCF suppressed miR-185-5p and upregulated its target NPHS2, with a net effect of alleviating renal interstitial fibrosis in CKD.

Adenosine A2A receptor modulates neuroimmune function through Th17/retinoid-related orphan receptor gamma t (RORγt) signaling in a BTBR T + Itpr3 tf /J mouse model of autism

2017 ◽  
Vol 36 ◽  
pp. 14-24 ◽  
Author(s):  
Mushtaq A. Ansari ◽  
Ahmed Nadeem ◽  
Sabry M. Attia ◽  
Saleh A. Bakheet ◽  
Mohammad Raish ◽  
...  
Keyword(s):  
Mouse Model ◽  
Adenosine A2a Receptor ◽  
Orphan Receptor ◽  
A2a Receptor ◽  
Adenosine A2a

Inhibition of Necroptosis Attenuates Kidney Inflammation and Interstitial Fibrosis Induced By Unilateral Ureteral Obstruction

2017 ◽  
Vol 46 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Xia Xiao ◽  
Chunyang Du ◽  
Zhe Yan ◽  
Yonghong Shi ◽  
Huijun Duan ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Potential Role ◽  
Interstitial Fibrosis ◽  
Kidney Diseases ◽  
Specific Inhibitor ◽  
Unilateral Ureteral Obstruction ◽  
Renal Diseases ◽  
Renal Interstitial Fibrosis ◽  
Renal Inflammation ◽  
Renal Histology

Background: Inflammation plays a crucial role in renal interstitial fibrosis, the pathway of chronic kidney diseases. Necroptosis is a novel form of regulated cell death, which plays a potential role in inflammation and renal diseases. The small molecule necrostatin-1 (Nec-1) is a specific inhibitor of necroptosis. This study was aimed at determining the role of necroptosis, RIP1/RIP3/mixed lineage kinase domain-like (MLKL) signaling pathway, in renal inflammation and interstitial fibrosis related to primitive tubulointerstitial injury. It was also aimed at evaluating the effect of Nec-1 in renal fibrosis induced by unilateral ureteral obstruction (UUO). Methods: Renal histology, immunohistochemistry, western blot, and real-time polymerase chain reaction were performed using UUO C57BL/6J mice model. Moreover, we tested whether Nec-1 was renal-protective in the interstitial fibrosis kidney. Mice were exposed to UUO and injected intraperitoneal with Nec-1 or vehicle. Results: The levels of RIP1/RIP3/MLKL protein and mRNA were increased in the obstructed kidneys 7 days after UUO; this was accompanied by changes in renal pathological lesions. Renal histological examination showed lesser renal damage in Nec-1-treated UUO mice. Renal inflammation, assessed by tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein-1 was markedly attenuated by Nec-1. Furthermore, Nec-1 treatment also significantly reduced TGF-β and α-smooth muscle actin, indicating lesser renal interstitial fibrosis. Conclusion: These findings suggest that the participation of necroptosis in UUO is partly demonstrated. And necroptosis inhibition may have a potential role in the treatment of diseases with increased inflammatory response and interstitial fibrosis in renal.

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