PRMT1-Orchestrated Fibroblast Activation in Renal Fibrosis Induced by TGFß/Smad3 Signaling Pathway

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2197-PUB
Author(s):  
YU ZHU ◽  
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Fibroblast Activation

Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro

2020 ◽  
Vol 21 (11) ◽  
pp. 1107-1118
Author(s):  
Ningning Li ◽  
Zhan Wang ◽  
Tao Sun ◽  
Yanfei Lei ◽  
Xianghua Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Therapeutic Potential ◽  
Protective Role ◽  
Fibroblast Proliferation ◽  
Fibroblast Activation ◽  
And Function ◽  
Activated Fibroblasts ◽  
Tgf Β1

Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast differentiation induced by TGF-β1. Result: Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. Conclusion: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis.

scholarly journals Blocking the Class I Histone Deacetylase Ameliorates Renal Fibrosis and Inhibits Renal Fibroblast Activation via Modulating TGF-Beta and EGFR Signaling

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54001 ◽  
Author(s):  
Na Liu ◽  
Song He ◽  
Li Ma ◽  
Murugavel Ponnusamy ◽  
Jinhua Tang ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Renal Fibrosis ◽  
Class I ◽  
Tgf Beta ◽  
Egfr Signaling ◽  
Fibroblast Activation

scholarly journals β-Catenin-Dependent Signaling Pathway Contributes to Renal Fibrosis in Hypertensive Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Catherina A. Cuevas ◽  
Cheril Tapia-Rojas ◽  
Carlos Cespedes ◽  
Nibaldo C. Inestrosa ◽  
Carlos P. Vio
Keyword(s):  
Blood Pressure ◽  
Signal Transduction ◽  
Single Dose ◽  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Target Genes ◽  
Hypertensive Rats ◽  
Collagen Types ◽  
Dependent Signaling Pathway ◽  
Pyrvinium Pamoate

The mechanism of hypertension-induced renal fibrosis is not well understood, although it is established that high levels of angiotensin II contribute to the effect. Sinceβ-catenin signal transduction participates in fibrotic processes, we evaluated the contribution ofβ-catenin-dependent signaling pathway in hypertension-induced renal fibrosis. Two-kidney one-clip (2K1C) hypertensive rats were treated with lisinopril (10 mg/kg/day for four weeks) or with pyrvinium pamoate (Wnt signaling inhibitor, single dose of 60 ug/kg, every 3 days for 2 weeks). The treatment with lisinopril reduced the systolic blood pressure from 220 ± 4 in 2K1C rats to 112 ± 5 mmHg (P<0.05), whereas the reduction in blood pressure with pyrvinium pamoate was not significant (212 ± 6 in 2K1C rats to 170 ± 3 mmHg,P>0.05). The levels of collagen types I and III, osteopontin, and fibronectin decreased in the unclipped kidney in both treatments compared with 2K1C rats. The expressions ofβ-catenin, p-Ser9-GSK-3beta, and theβ-catenin target genes cyclin D1, c-myc, and bcl-2 significantly decreased in unclipped kidney in both treatments (P<0.05). In this study we provided evidence thatβ-catenin-dependent signaling pathway participates in the renal fibrosis induced in 2K1C rats.

Tubule‐derived INHBB promotes interstitial fibroblast activation and renal fibrosis

2021 ◽  
Author(s):  
Yanyan Sun ◽  
Huimin Cai ◽  
Jia Ge ◽  
Fang Shao ◽  
Zhen Huang ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Fibroblast Activation

scholarly journals miR-136 improves renal fibrosis in diabetic rats by targeting down-regulation of tyrosine kinase SYK and inhibition of TGF-β1/Smad3 signaling pathway

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 513-522 ◽  
Author(s):  
Lei Liu ◽  
Xinlu Pang ◽  
Wenjun Shang ◽  
Guiwen Feng ◽  
Zhigang Wang ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Diabetic Rats ◽  
Down Regulation ◽  
Tgf Β1

Silibinin enhances anti-renal fibrosis effect of MK-521 via downregulation of TGF-β signaling pathway

Human Cell ◽  
2020 ◽  
Vol 33 (2) ◽  
pp. 330-336 ◽  
Author(s):  
Zhongchao Ma ◽  
Wenwen Zang ◽  
Huaiguo Wang ◽  
Xiaojing Wei
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis

scholarly journals Kaempferol Protects Renal Fibrosis through Activating the BMP-7-Smad1/5 Signaling Pathway

2020 ◽  
Vol 43 (3) ◽  
pp. 533-539
Author(s):  
Xiaojun Ji ◽  
Jing Cao ◽  
Liting Zhang ◽  
Zhirui Zhang ◽  
Weiwei Shuai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis

scholarly journals Effects of dexmedetomidine on the RhoA /ROCK/ Nox4 signaling pathway in renal fibrosis of diabetic rats

Open Medicine ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. 890-898 ◽  
Author(s):  
Chen Jihua ◽  
Chen Cai ◽  
Bao Xubin ◽  
Yu Yue
Keyword(s):  
Renal Function ◽  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Rat Kidney ◽  
Diabetic Rats ◽  
Immunohistochemical Method ◽  
Model Group ◽  
Protein Expressions ◽  
Masson Staining

AbstractObjectiveTo investigate the effects and mechanisms of dexmedetomidine (Dex) on model rats of diabetic nephropathy (DN).MethodsRats were divided into NC, model, Dex-L (1μg/ kg), Dex-M (5μg/kg) and Dex-H (10μg/kg) groups. Rats in all groups except in the NC group were injected with streptozotocin (STZ) combined with right nephrectomy. Rats in Dex (1, 5 and 10μg/kg) groups received gavage with Dex (1, 5 and 10μg/kg). After 4 weeks, rats were sacrificed and kidneys were collected. HE staining was performed for a renal injury. Masson staining was applied to detect the fibrotic accumulation in rat kidney. Radioimmunoassay was used to test the renal function. Immunohistochemical method was used to detect protein expressions of RhoA, p-MYPT and Nox4 in rat kidney.ResultsCompared with the NC group, the levels of urine microalbumin in protein, α1-MG and β2-MG, renal fibrotic accumulation, RhoA, p-MYPT, Nox4 and α-SMA in model group increased significantly (P＜0.001, respectively). Compared with the model group, Dex low, medium and high groups improved the deposition of renal fiber in rats, inhibited the expression levels of microalbumin, α1-MG and β2-MG in urine and decreased expression of RhoA, p-MYPT, Nox4 and α-SMA proteins (P＜0.05, P＜0.01).ConclusionDex is possible to inhibit the expression of α-SMA and renal fibrous substance deposition in rat kidney via RhoA/ROCK/Nox4 signaling pathway, thereby reducing early kidney damage in model rats.

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