ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling.
Adipose Tissue
/ metabolism
Adult
Aged
Aged, 80 and over
Chemokine CCL2
/ genetics
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Female
Gene Expression
/ drug effects
Humans
Hydrogen Peroxide
/ pharmacology
Interleukin-8
/ genetics
Male
Middle Aged
Monocytes
/ drug effects
NF-kappa B
/ metabolism
Reactive Oxygen Species
/ metabolism
Signal Transduction
/ drug effects
THP-1 Cells
Tumor Necrosis Factor-alpha
/ pharmacology
CCL2
CXCL8
IL-8
MCP-1
ROS
TNF-α
meta-inflammation
obesity
oxidative stress
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
29 Sep 2021
29 Sep 2021
Historique:
received:
18
08
2021
revised:
15
09
2021
accepted:
22
09
2021
entrez:
13
10
2021
pubmed:
14
10
2021
medline:
3
11
2021
Statut:
epublish
Résumé
IL-8/MCP-1 act as neutrophil/monocyte chemoattractants, respectively. Oxidative stress emerges as a key player in the pathophysiology of obesity. However, it remains unclear whether the TNF-α/oxidative stress interplay can trigger IL-8/MCP-1 expression and, if so, by which mechanism(s). IL-8/MCP-1 adipose expression was detected in lean, overweight, and obese individuals, 15 each, using immunohistochemistry. To detect the role of reactive oxygen species (ROS)/TNF-α synergy as a chemokine driver, THP-1 cells were stimulated with TNF-α, with/without H
Identifiants
pubmed: 34638857
pii: ijms221910519
doi: 10.3390/ijms221910519
pmc: PMC8508672
pii:
doi:
Substances chimiques
CCL2 protein, human
0
Chemokine CCL2
0
Interleukin-8
0
NF-kappa B
0
Reactive Oxygen Species
0
Tumor Necrosis Factor-alpha
0
Hydrogen Peroxide
BBX060AN9V
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Kuwait Foundation for the Advancement of Sciences
ID : RA HM-2019-022; RA 2010-003
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