scholarly journals Microarray Analysis Reveals Increased Expression of Matrix Metalloproteases and Cytokines of Interleukin-20 Subfamily in the Kidneys of Neonate Rats Underwent Unilateral Ureteral Obstruction: A Potential Role of IL-24 in the Regulation of Inflammation and Tissue Remodeling

2017 ◽  
Vol 42 (1) ◽  
pp. 16-32 ◽  
Author(s):  
Domonkos Pap ◽  
Erna Sziksz ◽  
Zoltán Kiss ◽  
Réka Rokonay ◽  
Apor Veres-Székely ◽  
...  
Keyword(s):  
Microarray Analysis ◽  
Ureteral Obstruction ◽  
Potential Role ◽  
Tissue Remodeling ◽  
Unilateral Ureteral Obstruction ◽  
Matrix Metalloproteases

scholarly journals Potential Role of the Resident Mesenchymal Stem-Like Cells in Renal Fibrogenesis after Ureteral Obstruction

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Yong-Hua Peng ◽  
Jie Xiao ◽  
Chen Yan ◽  
Lan Luo ◽  
Tao-Sheng Li
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Ureteral Obstruction ◽  
Potential Role ◽  
Histological Analysis ◽  
Left Kidney ◽  
Inflammatory Cells ◽  
Unilateral Ureteral Obstruction ◽  
Renal Fibrogenesis

The mechanisms of renal fibrogenesis after ureteral obstruction remain unclear. We tried to primarily expand mesenchymal stem cells from renal tissues and then investigated their role in fibrogenesis after ureteral obstruction. Unilateral ureteral obstruction was induced by ligating the left ureteral duct of adult C57BL/6 mice. We collected the kidneys for experiments at 2, 7, and 14 days after operation. Histological analysis showed obviously fibrotic changes in the left kidney at 7 days and further increased at 14 days after ureteral obstruction. To expand mesenchymal stem cells, we minced the renal tissues into small explants (about 1 mm3) and cultured onto 10 cm dishes. Interestingly, the outgrowth of cells was observed significantly earlier from the explants of the obstructed left kidney than that of the unobstructed right kidney. These expanded cells showed the potency of adipogenic, osteogenic, and chondrogenic differentiations and positively expressed with CD44 and partly expressed with CD90, CD105, and CD106, but negatively expressed with CD34, CD45, and FSP1, suggesting the phenotype of mesenchymal stem-like cells (MSLCs). The mouse fibrosis RT2 profiler PCR array showed that many genes were changed over 2-fold in the MSLCs expanded from both kidneys at 2, 7, and 14 days after operation. Interestingly, profibrotic genes were prevalently enhanced in the left kidney with ureteral obstruction. Histological analysis also showed obviously infiltration of inflammatory cells in the left kidney at 14 days after operation. Our data indicate the potential role of resident MSLCs in renal fibrogenesis after ureteral obstruction, but further experiments are required to understand the relevant mechanisms.

scholarly journals The Role of Apelin on the Alleviative Effect of Angiotensin Receptor Blocker in Unilateral Ureteral Obstruction-Induced Renal Fibrosis

Nephron Extra ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Masashi Nishida ◽  
Yasuko Okumura ◽  
Tatsujiro Oka ◽  
Kentaro Toiyama ◽  
Seiichiro Ozawa ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Angiotensin Receptor Blocker ◽  
Unilateral Ureteral Obstruction ◽  
Receptor Blocker ◽  
Angiotensin Receptor

scholarly journals Role of Sirolimus in renal tubular apoptosis in response to unilateral ureteral obstruction

2018 ◽  
Vol 15 (13) ◽  
pp. 1433-1442 ◽  
Author(s):  
Mei Yang ◽  
Yang-yang Zhuang ◽  
Wei-wei Wang ◽  
Hai-ping Zhu ◽  
Yan-jie Zhang ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Renal Tubular

scholarly journals Correction: Role of the high-affinity leukotriene B4 receptor signaling in fibrosis after unilateral ureteral obstruction in mice

PLoS ONE ◽  
2019 ◽  
Vol 14 (4) ◽  
pp. e0215625
Author(s):  
Mariko Kamata ◽  
Hideki Amano ◽  
Yoshiya Ito ◽  
Tomoe Fujita ◽  
Fumisato Otaka ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Leukotriene B4 ◽  
Unilateral Ureteral Obstruction ◽  
Receptor Signaling ◽  
High Affinity ◽  
Leukotriene B4 Receptor

scholarly journals Long-term renal effects of unilateral ureteral obstruction and the role of endothelin

2000 ◽  
Vol 58 (1) ◽  
pp. 242-250 ◽  
Author(s):  
Fayez T. Hammad ◽  
Antony M. Wheatley ◽  
Gerard Davis
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Renal Effects

scholarly journals Tempol Attenuates Renal Fibrosis in Mice with Unilateral Ureteral Obstruction: The Role of PI3K-Akt-FoxO3a Signaling

2014 ◽  
Vol 29 (2) ◽  
pp. 230 ◽  
Author(s):  
Hye Eun Yoon ◽  
Soo Jeong Kim ◽  
Sung Jun Kim ◽  
Sungjin Chung ◽  
Seok Joon Shin
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Unilateral Ureteral Obstruction

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.

Cellular distribution of H(+)-ATPase following acute unilateral ureteral obstruction in rats

1991 ◽  
Vol 261 (3) ◽  
pp. F365-F376 ◽  
Author(s):  
H. Purcell ◽  
B. Bastani ◽  
K. P. Harris ◽  
P. Hemken ◽  
S. Klahr ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Morphological Changes ◽  
Rat Kidney ◽  
Cell Number ◽  
Unilateral Ureteral Obstruction ◽  
Cellular Distribution ◽  
Physiological Abnormalities ◽  
Human Disorder ◽  
Atpase Staining

Unilateral ureteral obstruction for 24 h produces an acidification defect in the rat kidney that closely resembles the human disorder. We examined the role of renal vacuolar H(+)-ATPase distribution and content in the generation of the postobstructive abnormality in distal hydrogen ion secretion. Rats were subjected to unilateral ureteral obstruction for 24 h, and the obstructed and contralateral kidneys were removed at 3 h, 5 days, and 10 days after release of the obstruction. The postobstructed and contralateral kidneys and kidneys from sham-operated rats were analyzed for intercalated cell number and subtype and for the cellular distribution of ATPase staining by means of a monoclonal antibody specific for the 31-kDa subunit of the vacuolar H(+)-ATPase. No change in the number or distribution of subtypes was detected in the cortex nor in the outer or inner stripe of the outer medulla. Immunoreactive H(+)-ATPase increased in both the cortex and medulla at 3 h after obstruction, and thereafter it declined to control values. The major morphological changes in H(+)-ATPase staining detected were an alteration in the intracellular distribution of the enzyme, which we refer to as discontinuity of (or “gaps” in) apical staining, and a decrease in the percent of intercalated cells showing a rim (or plasma membrane) staining pattern in the inner medulla. The changes observed may be a morphological representation of the physiological abnormalities underlying the postobstructive acidification defect.

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