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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway
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Advanced glycation endproducts increase EPC apoptosis and decrease nitric oxide release via MAPK pathways.

C Shen1, Q Li, Y C Zhang

  • 1Department of Cardiology, Zhongda Hospital, Southeast University; Nanjing, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|September 22, 2009
PubMed
Summary
This summary is machine-generated.

Advanced glycation endproducts (AGE) induce endothelial progenitor cell (EPC) apoptosis and reduce nitric oxide (NO) release. These effects are mediated through mitogen-activated protein kinase (MAPK) pathways, highlighting a potential therapeutic target.

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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
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Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway
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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Diabetes Pathogenesis

Background:

  • Advanced glycation endproducts (AGE) are implicated in diabetic complications.
  • AGE-induced endothelial progenitor cell (EPC) apoptosis contributes to diabetes mellitus pathogenesis.
  • Nitric oxide (NO) signaling is crucial in regulating apoptosis.

Purpose of the Study:

  • To investigate the impact of AGE on human EPC apoptosis and NO release.
  • To elucidate the role of mitogen-activated protein kinase (MAPK) pathways in AGE-induced EPC apoptosis.

Main Methods:

  • Human EPCs were cultured with varying AGE concentrations and durations.
  • EPC apoptosis and NO release were quantified.
  • mRNA and protein expression of key apoptotic and signaling molecules (eNOS, COX-2, Bcl-2, Bax, NF-kappaB, Caspase-3) were analyzed.
  • MAPK inhibitors were used to assess pathway involvement.

Main Results:

  • High AGE concentration (200mg/L) significantly increased EPC apoptosis and decreased NO release in a time-dependent manner.
  • AGE exposure altered the expression of eNOS, Bcl-2, COX-2, Bax, NF-kappaB, and Caspase-3.
  • MAPK pathway inhibition attenuated AGE-induced EPC apoptosis and molecular changes.

Conclusions:

  • AGE promotes EPC apoptosis and reduces NO release.
  • The MAPK signaling pathway is a key mediator of AGE's effects on EPCs.
  • Targeting MAPK pathways may offer a therapeutic strategy for diabetic vascular complications.