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Erschienen in: Inflammation 5/2014

01.10.2014

Exendin-4 Inhibits HMGB1-Induced Inflammatory Responses in HUVECs and in Murine Polymicrobial Sepsis

verfasst von: Wonhwa Lee, Sae-Kwang Ku, Eun Ji Park, Dong Hee Na, Kyung-Min Kim, Jong-Sup Bae

Erschienen in: Inflammation | Ausgabe 5/2014

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Abstract

Exendin-4 (EX4) has been reported to attenuate myocardial ischemia and reperfusion (I/R) injury and inflammatory and oxidative responses. Nuclear DNA-binding protein high-mobility group box 1 (HMGB1) protein acts as a late mediator of severe vascular inflammatory conditions. However, the effect of EX4 on HMGB1-induced inflammatory response has not been studied. First, we accessed this question by monitoring the effects of posttreatment EX4 on lipopolysaccharide (LPS) and cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated regulation of proinflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice. Posttreatment EX4 was found to suppress LPS-mediated release of HMGB1 and inhibited HMGB1-mediated hyperpermeability and leukocyte migration in septic mice. EX4 also induced downregulation of CLP-induced release of HMGB1, production of IL-6, and mortality. Collectively, these results suggest that EX4 may be regarded as a candidate therapeutic agent for treatment of vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway.
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Metadaten
Titel
Exendin-4 Inhibits HMGB1-Induced Inflammatory Responses in HUVECs and in Murine Polymicrobial Sepsis
verfasst von
Wonhwa Lee
Sae-Kwang Ku
Eun Ji Park
Dong Hee Na
Kyung-Min Kim
Jong-Sup Bae
Publikationsdatum
01.10.2014
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 5/2014
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-014-9919-9

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