934 EDARAVONE, A RADICAL SCAVENGER, INHIBITS CISPLATIN-INDUCED ACUTE RENAL INJURY AND CHRONIC RENAL CYST FORMATION BY PROTECTING RENAL MITOCHONDRIA

2010 ◽  
Vol 9 (2) ◽  
pp. 293
Author(s):  
T. Iguchi ◽  
M. Nishikawa ◽  
M. Inoue ◽  
Y. Nitta ◽  
T. Naganuma ◽  
...  
2019 ◽  
Vol 30 (10) ◽  
pp. 1841-1856 ◽  
Author(s):  
Kurt A. Zimmerman ◽  
Cheng J. Song ◽  
Zhang Li ◽  
Jeremie M. Lever ◽  
David K. Crossman ◽  
...  

BackgroundMutations affecting cilia proteins have an established role in renal cyst formation. In mice, the rate of cystogenesis is influenced by the age at which cilia dysfunction occurs and whether the kidney has been injured. Disruption of cilia function before postnatal day 12–14 results in rapid cyst formation; however, cyst formation is slower when cilia dysfunction is induced after postnatal day 14. Rapid cyst formation can also be induced in conditional adult cilia mutant mice by introducing renal injury. Previous studies indicate that macrophages are involved in cyst formation, however the specific role and type of macrophages responsible has not been clarified.MethodsWe analyzed resident macrophage number and subtypes during postnatal renal maturation and after renal injury in control and conditional Ift88 cilia mutant mice. We also used a pharmacological inhibitor of resident macrophage proliferation and accumulation to determine the importance of these cells during rapid cyst formation.ResultsOur data show that renal resident macrophages undergo a phenotypic switch from R2b (CD11clo) to R2a (CD11chi) during postnatal renal maturation. The timing of this switch correlates with the period in which cyst formation transitions from rapid to slow following induction of cilia dysfunction. Renal injury induces the reaccumulation of juvenile-like R2b resident macrophages in cilia mutant mice and restores rapid cystogenesis. Loss of primary cilia in injured conditional Ift88 mice results in enhanced epithelial production of membrane-bound CSF1, a cytokine that promotes resident macrophage proliferation. Inhibiting CSF1/CSF1-receptor signaling with a CSF1R kinase inhibitor reduces resident macrophage proliferation, R2b resident macrophage accumulation, and renal cyst formation in two mouse models of cystic disease.ConclusionsThese data uncover an important pathogenic role for resident macrophages during rapid cyst progression.


2008 ◽  
Vol 179 (4S) ◽  
pp. 117-118
Author(s):  
Taro Iguchi ◽  
Manabu Nishikawa ◽  
Masayasu Inoue ◽  
Ching Y Wang ◽  
Gabriel P Haas ◽  
...  

2004 ◽  
Vol 38 (4) ◽  
pp. 333-341 ◽  
Author(s):  
Taro Iguchi ◽  
Manabu Nishikawa ◽  
BaoJun Chang ◽  
Osuke Muroya ◽  
Eisuke F sato ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Liu Tongqiang ◽  
Liu Shaopeng ◽  
Yu Xiaofang ◽  
Song Nana ◽  
Xu Xialian ◽  
...  

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.


2007 ◽  
Vol 33 (5) ◽  
pp. 550-555 ◽  
Author(s):  
M. Tallgren ◽  
T. Niemi ◽  
R. Pöyhiä ◽  
E. Raininko ◽  
M. Railo ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0141622 ◽  
Author(s):  
Jian-bo Yu ◽  
Jia Shi ◽  
Yuan Zhang ◽  
Li-rong Gong ◽  
Shu-an Dong ◽  
...  

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