Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure

Nephrology ◽  
2017 ◽  
Vol 22 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Asuka Baba ◽  
Masahiro Tachi ◽  
Yutaka Ejima ◽  
Yasuhiro Endo ◽  
Hiroaki Toyama ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Mast Cells ◽  
Renal Fibrosis ◽  
Rat Kidneys

Benidipine Suppresses in situ Proliferation of Leukocytes and Slows the Progression of Renal Fibrosis in Rat Kidneys with Advanced Chronic Renal Failure

2014 ◽  
Vol 128 (1-2) ◽  
pp. 67-79 ◽  
Author(s):  
Itsuro Kazama ◽  
Asuka Baba ◽  
Mitsunobu Matsubara ◽  
Yasuhiro Endo ◽  
Hiroaki Toyama ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Fibrosis ◽  
Rat Kidneys

scholarly journals Overexpression of Delayed RectifierK+Channels PromotesIn situProliferation of Leukocytes in Rat Kidneys with Advanced Chronic Renal Failure

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Itsuro Kazama ◽  
Yoshio Maruyama ◽  
Yasuhiro Endo ◽  
Hiroaki Toyama ◽  
Yutaka Ejima ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Fibrosis ◽  
Recovery Period ◽  
Cortical Cell ◽  
Delayed Rectifier ◽  
Kv1.3 Channel ◽  
Kv1.3 Channels ◽  
Rat Kidneys

Leukocytes, such as lymphocytes and macrophages, predominantly express delayed rectifier K+channels (Kv1.3), and the channels play crucial roles in the activation and proliferation of the cells. Since lymphocytes are activated in patients with end-stage renal disease (ESRD), the channels expressed in those cells would contribute to the progression of renal fibrosis in advanced-stage chronic renal failure (CRF). In the present study, using a rat model with advanced CRF that underwent 5/6 nephrectomy followed by a 14-week recovery period, we examined the histopathological features of the kidneys and the leukocyte expression of Kv1.3-channels and cell cycle markers. Age-matched sham-operated rats were used as controls. In the cortical interstitium of advanced CRF rat kidneys, leukocytes proliferatedin situand overexpressed Kv1.3 channel protein in their cytoplasm. Treatment with margatoxin, a selective Kv1.3-channel inhibitor, significantly suppressed the number of leukocytes and the progression of renal fibrosis with a significant decrease in the cortical cell cycle marker expression. This study demonstrated for the first time that the number of leukocytes was dramatically increased in rat kidneys with advanced CRF. The overexpression of Kv1.3 channels in the leukocytes was thought to contribute to the progression of renal fibrosis by stimulating cell cycling and promoting cellular proliferation.

scholarly journals The Dysregulation of Eicosanoids and Bile Acids Correlates with Impaired Kidney Function and Renal Fibrosis in Chronic Renal Failure

Metabolites ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 127
Author(s):  
Yan-Ni Wang ◽  
He-He Hu ◽  
Dan-Dan Zhang ◽  
Xia-Qing Wu ◽  
Jian-Ling Liu ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Bile Acids ◽  
Kidney Function ◽  
Linear Correlation ◽  
Renal Fibrosis ◽  
Bile Acid Metabolism ◽  
Operating Characteristics ◽  
Renal Functions ◽  
Lipid Species

Chronic renal failure (CRF) is an irreversible deterioration of the renal functions that characterized by fluid electrolyte unbalance and metabolic-endocrine dysfunctions. Increasing evidence demonstrated that metabolic disturbances, especially dyslipidemia and profound changes in lipid and lipoprotein metabolism were involved in CRF. Identification of lipids associated with impaired kidney functions may play important roles in the understanding of biochemical mechanism and CRF treatment. Ultra-performance liquid chromatography coupled with high-definition mass spectrometry-based lipidomics was performed to identify important differential lipids in adenine-induced CRF rats and investigate the undergoing anti-fibrotic mechanism of Polyporus umbellatus (PPU) and ergone (ERG). Linear correlation analysis was performed between lipid species intensities and creatinine levels in serum. Adenine-induced rats exhibited declining kidney function and renal fibrosis. Compared with control rats, a panel of lipid species was identified in the serum of CRF rats. Our further study demonstrated that eight lipids, including leukotrienes and bile acids, presented a strong linear correlation with serum creatinine levels. In addition, receiver operating characteristics analysis showed that eight lipids exhibited excellent area under the curve for differentiating CRF from control rats, with high sensitivity and specificity. The aberrant changes of clinical biochemistry data and dysregulation of eight lipids could be significantly improved by the administration of PPU and ergone. In conclusion, CRF might be associated with the disturbance of leukotriene metabolism, bile acid metabolism and lysophospholipid metabolism. The levels of eicosanoids and bile acids could be used for indicating kidney function impairment in CRF. PPU could improve renal functions and either fully or partially reversed the levels of eicosanoids and bile acids.

scholarly journals Inhibition of fibronectin polymerization alleviates kidney injury due to ischemia-reperfusion

2019 ◽  
Vol 316 (6) ◽  
pp. F1293-F1298 ◽  
Author(s):  
Stephanie L. K. Bowers ◽  
Stephanie Davis-Rodriguez ◽  
Zachary M. Thomas ◽  
Valeria Rudomanova ◽  
W. Clark Bacon ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Small Peptide ◽  
Relevant Model ◽  
Novel Approach

Fibrosis is a common feature of chronic kidney disease; however, no clinical therapies effectively target the progression of fibrosis. Inhibition of fibronectin polymerization with the small peptide pUR4 attenuates fibrosis in the liver and heart. Here, we show that pUR4 decreases renal fibrosis and tissue remodeling using a clinically relevant model of kidney injury, unilateral ischemia-reperfusion. This work highlights the benefits of inhibiting matrix polymerization, alone or in conjunction with cell-based therapies, as a novel approach to diminish the maladaptive responses to ischemic kidney injury that lead to chronic renal failure.

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