NOD2 induces VCAM-1 and ET-1 gene expression via NF-κB in human umbilical vein endothelial cells with muramyl dipeptide stimulation.
Herz
; 46(Suppl 2): 265-271, 2021 Sep.
Article
en En
| MEDLINE
| ID: mdl-33245410
ABSTRACT
OBJECTIVES:
Endothelial dysfunction is involved in various aspects of vascular biology and different stages of cardiovascular diseases (CVDs). Nucleotide-binding oligomerization domain-containing protein (NOD) 2, a pivotal innate immune receptor for muramyl dipeptide (MDP), has been reported to be a central regulator in CVDs. Previously, we reported that NOD2 played a leading role in MDP-triggered oxidative stress in endothelial cells (ECs). However, whether NOD2 participates in the regulatory mechanism of vascular cell adhesion molecule1 (VCAM-1) and endothelin1 (ET-1) expression was not elucidated.METHODS:
Human umbilical vein endothelial cells (HUVECs) were stimulated with MDP for 12â¯h. mRNA expression of VCAM1 and ET1 was detected using real time polymerase chain reaction (PCR). Scrambled control small interfering RNA (siRNA) and NOD2 siRNA were transfected into HUVECs using Lipofectamine 2000 reagent (Invitrogen, Waltham, MA, USA). Furthermore, pyrrolidine dithiocarbamate was adopted to investigate the effect of nuclear factor κB (NF-κB) on NOD2-mediated VCAM1 and ET1 gene expression in MDP-treated HUVECs.RESULTS:
Data showed that MDP significantly increased VCAM1 and ET1 mRNA expression, which was dependent on NOD2. In addition, NF-κB inhibition suppressed NOD2-mediated gene expression of VCAM1 and ET1.CONCLUSION:
Collectively, we confirmed NOD2 aggravated VCAM1 and ET1 gene expression through NF-κB in HUVECs treated with MDP.Palabras clave
Texto completo:
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Banco de datos:
MEDLINE
Asunto principal:
FN-kappa B
/
Molécula 1 de Adhesión Celular Vascular
Límite:
Humans
Idioma:
En
Año:
2021
Tipo del documento:
Article