N-methyl-D-aspartic acid increases tight junction protein destruction in brain endothelial cell via caveolin-1-associated ERK1/2 signaling

N-methyl-D-aspartic acid (NMDA), a glutamate analog, can activate N-Methyl-D-Aspartate receptor (NMDAR) to induce vascular endothelial cell injury but the mechanisms are not fully understood. The present study intended to evaluate the role of caveolin-1 (Cav-1) in NMDA-induced dysfunction of human b...

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Veröffentlicht in:	Toxicology (Amsterdam) 2022-03, Vol.470, p.153139-153139, Article 153139
Hauptverfasser:	Mao, Fengping, Huang, Fang, Nong, Weidong, Lao, Dayuan, Gong, Zhuowei, Huang, Wen
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals antagonists brain Brain - metabolism Caveolin 1 - genetics Caveolin 1 - metabolism Caveolin-1 electrical resistance Endothelial Cells ERK1/2 signaling genes glutamic acid Human cerebrovascular endothelial cells Humans MAP Kinase Signaling System Mice mitogen-activated protein kinase N-methyl-D-aspartic acid N-Methylaspartate - toxicity Receptors, N-Methyl-D-Aspartate - metabolism RNA, Small Interfering - pharmacology Signal Transduction Tight Junction Proteins tight junctions Tight Junctions - metabolism toxicology Western blotting ZO-1 Zonula Occludens-1 Protein - genetics Zonula Occludens-1 Protein - metabolism
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