MicroRNA-21 contributes to high glucose-induced fibrosis in peritoneal mesothelial cells in rat models by activation of the Ras-MAPK signaling pathway via Sprouty-1

2018 ◽  
Vol 234 (5) ◽  
pp. 5915-5925 ◽  
Author(s):  
Qing Gao ◽  
Lin Xu ◽  
Qian Yang ◽  
Tian-Jun Guan
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Mapk Signaling ◽  
Mesothelial Cells ◽  
Mapk Signaling Pathway ◽  
Rat Models ◽  
Peritoneal Mesothelial Cells

scholarly journals Adiponectin attenuates high glucose-induced apoptosis through the AMPK/p38 MAPK signaling pathway in NRK-52E cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0178215 ◽  
Author(s):  
Yuanyuan Wang ◽  
Juan Zhang ◽  
Lian Zhang ◽  
Ping Gao ◽  
Xiaoyan Wu
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
High Glucose ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Induced Apoptosis

scholarly journals Attenuation of High Glucose-Induced Damage in RPE Cells through p38 MAPK Signaling Pathway Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Grazia Maugeri ◽  
Claudio Bucolo ◽  
Filippo Drago ◽  
Settimio Rossi ◽  
Michelino Di Rosa ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
High Glucose ◽  
Retinal Pigment ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Rpe Cells ◽  
Cox 2

This study aimed to investigate the high glucose damage on human retinal pigment epithelial (RPE) cells, the role of p38 MAPK signaling pathway and how dimethyl fumarate can regulate that. We carried out in vitro studies on ARPE-19 cells exposed to physiological and high glucose (HG) conditions, to evaluate the effects of DMF on cell viability, apoptosis, and expression of inflammatory and angiogenic biomarkers such as COX-2, iNOS, IL-1β, and VEGF. Our data have demonstrated that DMF treatment attenuated HG-induced apoptosis, as confirmed by reduction of BAX/Bcl-2 ratio. Furthermore, in RPE cells exposed to HG we observed a significant increase of iNOS, COX-2, and IL-1β expression, that was reverted by DMF treatment. Moreover, DMF reduced the VEGF levels elicited by HG, inhibiting p38 MAPK signaling pathway. The present study demonstrated that DMF provides a remarkable protection against high glucose-induced damage in RPE cells through p38 MAPK inhibition and the subsequent down-regulation of VEGF levels, suggesting that DMF is a small molecule that represents a good candidate for diabetic retinopathy treatment and warrants further in vivo and clinical evaluation.

scholarly journals Ramipril inhibits high glucose-stimulated up-regulation of adhesion molecules via the ERK1/2 MAPK signaling pathway in human umbilical vein endothelial cells

2015 ◽  
Vol 20 (5) ◽  
Author(s):  
Moo Hyun Kim ◽  
Hae Min Kang ◽  
Chae-Eun Kim ◽  
Seongho Han ◽  
Sung-Whan Kim
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
High Glucose ◽  
Umbilical Vein ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

AbstractRamipril has recently been shown to have anti-atherogenic properties. However, the specific mechanisms underlying these effects remain unclear. The purpose of this study was to determine the effects of ramipril on induction of adhesion molecules in human umbilical vein endothelial cells (HUVECs) using high-glucose (HG) conditions and to investigate possible underlying molecular mechanisms. The effects of ramipril on expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 production, and ERK phosphorylation were examined in HG-induced HUVECs with inhibitors targeting the mitogen-activated protein kinase (MAPK) signaling pathway. HG induced the expression of the adhesion molecules ICAM-1 and VCAM-1. Pretreatment with ramipril drastically inhibited ICAM-1 and VCAM-1 production in a time- and dose-dependent manner. Moreover, upon investigating the effects of ramipril on the MAPK/extracellular signal-regulated kinase (ERK) signaling pathway, we found that ramipril completely inhibited HG-induced phosphorylation of ERK1/2. ERK inhibitors completely prevented the inhibitory effect of HG. This study demonstrated that ramipril reduces HG-stimulated induction of ICAM-1 and VCAM-1 expression via MAPK signaling, which may be useful for inhibition of atherosclerosis.

scholarly journals Tribbles 3 Regulates the Fibrosis Cytokine TGF-β1 through ERK1/2-MAPK Signaling Pathway in Diabetic Nephropathy

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Luwei Zhang ◽  
Jinhang Zhang ◽  
Xinnong Liu ◽  
Shengli Liu ◽  
Jun Tian
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
High Glucose ◽  
Collagen Type ◽  
Mesangial Cells ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Collagen Type Iv ◽  
Diabetic Mice ◽  
Type Iv

To reveal the expression and possible role of tribbles homolog 3 (TRB3) in the incidence of type 2 diabetic nephropathy, we used immunohistochemistry, real-time quantitative PCR, western blot analysis, and enzyme-linked immunosorbent assay (ELISA) to study the expression of TRB3, extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK), transforming growth factorβ1 (TGF-β1), and collagen type IV in kidneys of db/db diabetic mice and in murine renal mesangial cells stimulated with high glucose. The expression of TRB3, TGF-β1, and collagen type IV was increased in kidneys of db/db diabetic mice. TGF-β1 and collagen type IV regulated by high glucose through ERK1/2 MAPK were downregulated by silencing TRB3 in renal mesangial cells. TRB3 may be involved in diabetic nephropathy by regulating the fibrosis cytokine TGF-β1 and collagen type IV through the ERK1/2 MAPK signaling pathway.

scholarly journals Correction: Adiponectin attenuates high glucose-induced apoptosis through the AMPK/p38 MAPK signaling pathway in NRK-52E cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0182595
Author(s):  
Yuanyuan Wang ◽  
Juan Zhang ◽  
Lian Zhang ◽  
Ping Gao ◽  
Xiaoyan Wu
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
High Glucose ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Induced Apoptosis

MAPK: A Key Player in the Development and Progression of Stroke

2020 ◽  
Vol 19 (4) ◽  
pp. 248-256
Author(s):  
Yangmin Zheng ◽  
Ziping Han ◽  
Haiping Zhao ◽  
Yumin Luo
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Complex Disease ◽  
Therapeutic Targets ◽  
Cell Types ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Effective Prevention ◽  
Prevention And Treatment ◽  
Different Cell Types

Conclusion: Stroke is a complex disease caused by genetic and environmental factors, and its etiological mechanism has not been fully clarified yet, which brings great challenges to its effective prevention and treatment. MAPK signaling pathway regulates gene expression of eukaryotic cells and basic cellular processes such as cell proliferation, differentiation, migration, metabolism and apoptosis, which are considered as therapeutic targets for many diseases. Up to now, mounting evidence has shown that MAPK signaling pathway is involved in the pathogenesis and development of ischemic stroke. However, the upstream kinase and downstream kinase of MAPK signaling pathway are complex and the influencing factors are numerous, the exact role of MAPK signaling pathway in the pathogenesis of ischemic stroke has not been fully elucidated. MAPK signaling molecules in different cell types in the brain respond variously after stroke injury, therefore, the present review article is committed to summarizing the pathological process of different cell types participating in stroke, discussed the mechanism of MAPK participating in stroke. We further elucidated that MAPK signaling pathway molecules can be used as therapeutic targets for stroke, thus promoting the prevention and treatment of stroke.

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