| http://purl.uniprot.org/citations/27657826 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27657826 | http://www.w3.org/2000/01/rdf-schema#comment | "The AMP-activated protein kinase (AMPK) pathway has been shown to be able to regulate inflammation in several cell lines. We reported that fenoterol, a β2-adrenergic receptor (β2-AR) agonist, inhibited lipopolysaccharide (LPS)-induced AMPK activation and inflammatory cytokine production in THP-1 cells, a monocytic cell line in previous studies. 5-amino-1-β-d-ribofuranosyl-imidazole-4-carboxamide (AICAR) is an agonist of AMPK. Whether AICAR induced AMPK activation and inflammatory cytokine production in THP-1 cells can be inhibited by fenoterol is unknown. In this study, we explored the mechanism of β2-AR stimulation with fenoterol in AICAR-induced inflammatory cytokine secretion in THP-1 cells. We studied AMPK activation using p-AMPK and AMPK antibodies, nuclear factor-kappa B (NF-κB) activation and inflammatory cytokine secretion in THP-1 cells stimulated by β2-AR in the presence or absence of AICAR and small interfering RNA (siRNA)-mediated knockdown of β-arrestin-2 or AMPKα1 subunit. AICAR-induced AMPK activation, NF-κB activation and tumor necrosis factor (TNF)-α release were reduced by fenoterol. In addition, siRNA-mediated knockdown of β-arrestin-2 abolished fenoterol's inhibition of AICAR-induced AMPK activation and TNF-α release, thus β-arrestin-2 mediated the anti-inflammatory effects of fenoterol in AICAR-treated THP-1 cells. Furthermore, siRNA-mediated knockdown of AMPKα1 significantly attenuated AICAR-induced NF-κB activation and TNF-α release, so AMPKα1 was a key signaling molecule involved in AICAR-induced inflammatory cytokine production. These data suggested that fenoterol inhibited AICAR-induced AMPK activation and TNF-α release through β-arrestin-2 in THP-1 cells. Management especially inhibition of AMPK signaling may provide new approaches and strategies for the treatments of immune diseases including inflammatory diseases and other critical illness."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.biopha.2016.09.044"xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/author | "Chen J."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/author | "Xu J."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/author | "Wang W."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/author | "Li X.G."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/name | "Biomed Pharmacother"xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/pages | "185-190"xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/title | "Anti-inflammatory activities of fenoterol through beta-arrestin-2 and inhibition of AMPK and NF-kappaB activation in AICAR-induced THP-1 cells."xsd:string |
| http://purl.uniprot.org/citations/27657826 | http://purl.uniprot.org/core/volume | "84"xsd:string |
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