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Cited by 89Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressAntioxidant Activity and Oxidative Stress

Endothelial cell oxidative stress and signal transduction

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FONCEA, ROCIO, CARVAJAL, CRISTIAN, ALMARZA, CAROLINA, LEIGHTON, FEDERICO·2000·Biological Research
DOI 10.4067/s0716-97602000000200008
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Abstract

Endothelial dysfunction (ED) is an early event in atherosclerotic disease, preceding clinical manifestations and complications. Increased reactive oxygen species (ROS) have been implicated as important mechanisms that contribute to ED, and ROS's may function as intracellular messengers that modulate signaling pathways. Several intracellular signal events stimulated by ROS have been defined, including the identification of two members of the mitogen activated protein kinase family (ERK1/2 and big MAP kinase, BMK1), tyrosine kinases (Src and Syk) and different isoenzymes of PKC as redox-sensitive kinases. ROS regulation of signal transduction components include the modification in the activity of transcriptional factors such as NFkB and others that result in changes in gene expression and modifications in cellular responses. In order to understand the intracellular mechanisms induced by ROS in endothelial cells (EC), we are studying the response of human umbilical cord vein endothelial cells to increased ROS generation by different pro-atherogenic stimuli. Our results show that Homocysteine (Hcy) and oxidized LDL (oxLDL) enhance the activity and expression of oxidative stress markers, such as NFkB and heme oxygenase 1. These results suggest that these pro-atherogenic stimuli increase oxidative stress in EC, and thus explain the loss of endothelial function associated with the atherogenic process.

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  • Inflammatory signals such as LPS, pro-inflammatory cytokines, reactive oxygen species, advanced glycation end products, and oxidized LDL cause IKKβ phosphorylation; this phosphorylates IκBα, leading to its ubiquitination and degradation, which releases NF-κB to enter the nucleus and induce pro-inflammatory genes.

    “Extracellular inflammatory signals including lipopolysaccharide (LPS), pro-inflammatory cytokines, reactive oxygen species, advanced glycation end products, and oxidized low-density lipoprotein trigger the phosphorylation of IKKβ, which in turn phosphorylates IκBα for ubiquitination and degradation by proteasome [13–18].”

    From Edible blue-green algae reduce the production of pro-inflammatory cytokines by inhibiting NF-κB pathway in macrophages and splenocytes (2013) · cites this paper as [18]

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Authors
FONCEA, R., CARVAJAL, C., ALMARZA, C., & LEIGHTON, F.
Affiliations
Pontificia Universidad Católica de Chile (CL)
Corresponding author
FONCEA, ROCIO
Venue
Biological Research
Publisher
SciELO Agencia Nacional de Investigacion y Desarrollo (ANID)
Published
2000
Volume
33
Issue
2
Pages
89-96
ISSN
0716-9760 (ISSN-L)
DOI
10.4067/s0716-97602000000200008
OpenAlex
W2152725517
Cited by
89
References
0
Citations by year
2025: 2 · 2024: 3 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 6 · 2017: 5 · 2016: 4 · 2015: 5 · 2014: 8 · 2013: 10 · 2012: 3
FWCI
0.20
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Biological Research (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
  • Americanae (AECID Library) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
endothelial dysfunction, oxidative stress, reactive oxygen species, signal transduction, atherosclerosis, NF-κB, heme oxygenase-1, homocysteine, oxidized LDL, MAPK signaling, protein kinase C, Src kinase, Syk, human umbilical vein endothelial cells
MeSH terms
Arteriosclerosis, Homocysteine, Humans, Lipoproteins, LDL, Umbilical Veins, Signal Transduction, Gene Expression, Reactive Oxygen Species, Oxidative Stress, Hyperhomocysteinemia, Mitogen-Activated Protein Kinases, Endothelial Cells

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