scholarly journals Protective Role of Insulin-Like Growth Factor-1 Receptor in Endothelial Cells against Unilateral Ureteral Obstruction–Induced Renal Fibrosis

2015 ◽  
Vol 185 (5) ◽  
pp. 1234-1250 ◽  
Author(s):  
Ming Liang ◽  
Lauren E. Woodard ◽  
Anlin Liang ◽  
Jinlong Luo ◽  
Matthew H. Wilson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Protective Role ◽  
Unilateral Ureteral Obstruction ◽  
Insulin Like Growth Factor

Protective role of JAK/STAT signaling against renal fibrosis in mice with unilateral ureteral obstruction

2014 ◽  
Vol 150 (1) ◽  
pp. 78-87 ◽  
Author(s):  
Kiyomi Koike ◽  
Seiji Ueda ◽  
Sho-ichi Yamagishi ◽  
Hideo Yasukawa ◽  
Yusuke Kaida ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Protective Role ◽  
Unilateral Ureteral Obstruction ◽  
Stat Signaling

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 MON-218 Protective role of TV-induced autophagy in an in vivo model of unilateral ureteral obstruction-induced renal cell injury

2019 ◽  
Vol 4 (7) ◽  
pp. S390-S391
Author(s):  
D.E. Choi ◽  
K.W. Lee ◽  
K.R. Na ◽  
J.Y. Jeong ◽  
Y.R. Ham ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Cell ◽  
Cell Injury ◽  
Protective Role ◽  
Unilateral Ureteral Obstruction ◽  
In Vivo Model

Putative protective role of autoantibodies against the insulin-like growth factor-1 receptor in Graves’ Disease: results of a pilot study

2020 ◽  
Vol 43 (12) ◽  
pp. 1759-1768 ◽  
Author(s):  
G. Lanzolla ◽  
D. Ricci ◽  
F. Nicolì ◽  
E. Sabini ◽  
A. Sframeli ◽  
...  
Keyword(s):  
Pilot Study ◽  
Growth Factor ◽  
Protective Role ◽  
Graves Disease ◽  
Insulin Like Growth Factor

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

Evidence for a protective role of placental growth factor in cardiovascular disease

2020 ◽  
Vol 12 (572) ◽  
pp. eabc8587
Author(s):  
Yihong Chen ◽  
Anna Hultgårdh Nilsson ◽  
Isabel Goncalves ◽  
Andreas Edsfeldt ◽  
Gunnar Engström ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Lower Risk ◽  
Protective Role ◽  
Placental Growth Factor ◽  
Trail Receptor ◽  
Population Cohort

Placental growth factor (PlGF) is a mitogen for endothelial cells, but it can also act as a proinflammatory cytokine. Because it promotes early stages of plaque formation in experimental models of atherosclerosis and was implicated in epidemiological associations with risk of cardiovascular disease (CVD), PlGF has been attributed a pro-atherogenic role. Here, we investigated whether PlGF has a protective role in CVD and whether elevated PlGF reflects activation of repair processes in response to vascular stress. In a population cohort of 4742 individuals with 20 years of follow-up, high baseline plasma PlGF was associated with increased risk of cardiovascular death, myocardial infarction, and stroke, but these associations were lost or weakened when adjusting for cardiovascular risk factors known to cause vascular stress. Exposure of cultured endothelial cells to high glucose, oxidized low-density lipoprotein (LDL) or an inducer of apoptosis enhanced the release of PlGF. Smooth muscle cells and endothelial cells treated with PlGF small interference RNA demonstrated that autocrine PlGF stimulation plays an important role in vascular repair responses. High expression of PlGF in human carotid plaques removed at surgery was associated with a more stable plaque phenotype and a lower risk of future cardiovascular events. When adjusting associations of PlGF with cardiovascular risk in the population cohort for plasma soluble tumor necrosis factor–related apoptosis–inducing ligand (TRAIL) receptor-2, a biomarker of cellular stress, a high PlGF/TRAIL receptor-2 ratio was associated with a lower risk. Our findings provide evidence for a protective role of PlGF in CVD.

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

2018 ◽  
Author(s):  
Mariko Kamata ◽  
Hideki Amano ◽  
Yoshiya Ito ◽  
Tomoe Fujita ◽  
Kanako Hosono ◽  
...  
Keyword(s):  
Growth Factor ◽  
Ureteral Obstruction ◽  
Type I Collagen ◽  
Critical Role ◽  
Unilateral Ureteral Obstruction ◽  
Type I ◽  
Renal Tubules ◽  
Kidney Fibrosis ◽  
High Affinity

AbstractLeukotriene B4 (LTB4) is a lipid mediator that acts as a potent chemoattractant for inflammatory leukocytes. Kidney fibrosis is caused by migrating inflammatory cells and kidney-resident cells. Here, we examined the role of the high-affinity LTB4 receptor BLT1 during development of kidney fibrosis in wild-type (WT) mice and BLT1 knockout (BLT1-/-) mice with unilateral ureteral obstruction (UUO). We found elevated expression of 5-lipoxygenase (5-LOX), which generates LTB4, in the renal tubules of WT and BLT1-/- UUO mice. Accumulation of immunoreactive type I collagen in UUO kidneys of WT mice increased over time; however, the increase was less prominent in BLT1-/- mice. Accumulation of S100A4-positive fibroblasts also increased temporally in WT UUO kidneys, but was again less pronounced in those of BLT1-/- mice. The same was true of mRNA encoding transforming growth factor-β (TGF)-β and fibroblast growth factor (FGF)-2. Finally, accumulation of F4/80-positive macrophages, which secrete TGF-β, also increased temporally in WT UUO and BLT1-/- kidneys, but to a lesser extent in the latter. Following LTB4 stimulation in vitro, macrophages showed increased expression of mRNA encoding TGF-β/FGF-2 and Col1a1, whereas L929 fibroblasts showed increased expression of mRNA encoding α smooth muscle actin (SMA). Bone marrow (BM) transplantation studies revealed that the area positive for type I collagen was significantly smaller in BLT1-/--BM→WT UUO kidneys than in WT-BM→WT kidneys. Thus, LTB4-BLT1 signaling plays a critical role in fibrosis in UUO kidneys by increasing accumulation of macrophages and fibroblasts. Therefore, blocking BLT1 may prevent renal fibrosis.

scholarly journals Peroxidasin and eosinophil peroxidase, but not myeloperoxidase, contribute to renal fibrosis in the murine unilateral ureteral obstruction model

2019 ◽  
Vol 316 (2) ◽  
pp. F360-F371 ◽  
Author(s):  
Selene Colon ◽  
Haiyan Luan ◽  
Yan Liu ◽  
Cameron Meyer ◽  
Leslie Gewin ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Hypochlorous Acid ◽  
Unilateral Ureteral Obstruction ◽  
Tubulointerstitial Fibrosis ◽  
Renal Inflammation ◽  
Eosinophil Peroxidase ◽  
Hypohalous Acids ◽  
Heme Peroxidases

Renal fibrosis is the pathological hallmark of chronic kidney disease (CKD) and manifests as glomerulosclerosis and tubulointerstitial fibrosis. Reactive oxygen species contribute significantly to renal inflammation and fibrosis, but most research has focused on superoxide and hydrogen peroxide (H2O2). The animal heme peroxidases myeloperoxidase (MPO), eosinophil peroxidase (EPX), and peroxidasin (PXDN) uniquely metabolize H2O2 into highly reactive and destructive hypohalous acids, such as hypobromous and hypochlorous acid. However, the role of these peroxidases and their downstream hypohalous acids in the pathogenesis of renal fibrosis is unclear. Our study defines the contribution of MPO, EPX, and PXDN to renal inflammation and tubulointerstitial fibrosis in the murine unilateral ureteral obstruction (UUO) model. Using a nonspecific inhibitor of animal heme peroxidases and peroxidase-specific knockout mice, we find that loss of EPX or PXDN, but not MPO, reduces renal fibrosis. Furthermore, we demonstrate that eosinophils, the source of EPX, accumulate in the renal interstitium after UUO. These findings point to EPX and PXDN as potential therapeutic targets for renal fibrosis and CKD and suggest that eosinophils modulate the response to renal injury.

scholarly journals Renoprotective Effects of Maslinic Acid on Experimental Renal Fibrosis in Unilateral Ureteral Obstruction Model via Targeting MyD88

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenjuan Sun ◽  
Chang Hyun Byon ◽  
Dong Hyun Kim ◽  
Hoon In Choi ◽  
Jung Sun Park ◽  
...  
Keyword(s):  
Growth Factor ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Adaptor Protein ◽  
Tissue Growth ◽  
Unilateral Ureteral Obstruction ◽  
Maslinic Acid

Maslinic acid (MA), also named crategolic acid, is a pentacyclic triterpene extracted from fruits and vegetables. Although various beneficial pharmacological effects of MA have been revealed, its effect on renal fibrosis remains unclear. This study was designed to clarify whether MA could attenuate renal fibrosis and determine the putative underlying molecular mechanisms. We demonstrated that MA-treated mice with unilateral ureteral obstruction (UUO) developed a histological injury of low severity and exhibited downregulated expression of fibrotic markers, including α-smooth muscle actin (α-SMA), vimentin, and fibronectin by 38, 44 and 40%, and upregulated expression of E-cadherin by 70% as compared with untreated UUO mice. Moreover, MA treatment restored the expression levels of α-SMA, connective tissue growth factor, and vimentin to 10, 7.8 and 38% of those induced by transforming growth factor (TGF)-β in NRK49F cells. MA decreased expression of Smad2/3 phosphorylation and Smad4 in UUO kidneys and TGF-β treated NRK49F cells (p < 0.05, respectively). Notably, MA specifically interferes with MyD88, an adaptor protein, thereby mitigating Smad4 nuclear expression (p < 0.01 compared to TGF-β treated group) and ameliorating renal fibrotic changes (p < 0.01 for each fibrotic markers compared to TGF-β induced cells). In addition, in the UUO model and lipopolysaccharide-induced NRK49F cells, MA treatment decreased the expression of IL-1β, TGF-α and MCP-1, ICAM-1, associated with the suppression of NF-κB signaling. These findings suggest that MA is a potential agent that can reduce renal interstitial fibrosis, to some extent, via targeting TGF-β/Smad and MyD88 signaling.

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