Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 4322-4326, 2013.
Article
Dans Anglais
| WPRIM
| ID: wpr-327578
ABSTRACT
<p><b>BACKGROUND</b>Human antigen R (HuR) is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2) and HuR participate in the tumor necrosis factor (TNF)-induced expression of interleukin-6 (IL-6).</p><p><b>METHODS</b>Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNA-mediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points. The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting.</p><p><b>RESULTS</b>MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm.</p><p><b>CONCLUSIONS</b>MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR.</p>
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Pharmacologie
/
Lignée cellulaire
/
Interleukine-6
/
Facteur de nécrose tumorale alpha
/
Protein-Serine-Threonine Kinases
/
Protéines et peptides de signalisation intracellulaire
/
Antigènes Hu de l'encéphalomyélite paranéoplasique
/
Lésion pulmonaire aigüe
/
Génétique
/
Métabolisme
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Chinese Medical Journal
Année:
2013
Type:
Article
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