Mixed Lineage Kinase Domain-Like Protein Promotes Human Monocyte Cell Adhesion to Human Umbilical Vein Endothelial Cells Via Upregulation of Intercellular Adhesion Molecule-1 Expression.
Med Sci Monit
; 26: e924242, 2020 Aug 13.
Article
em En
| MEDLINE
| ID: mdl-32788571
ABSTRACT
BACKGROUND Atherosclerosis is a progressive inflammatory disease that involves a variety of inflammatory and proinflammatory factors, including intercellular adhesion molecule (ICAM)-1. ICAM-1 plays an important role in atherosclerosis by promoting cell adhesion. Mixed lineage kinase domain-like (MLKL), a critical regulator of necroptotic cell death, is indicated to play an important role in atherosclerosis. This study investigated the effects of MLKL on ICAM-1 expression and cell adhesion, thus providing a new direction for the research of atherosclerosis pathogenesis. MATERIAL AND METHODS siRNA-MLKL and pcDNA-MLKL were designed, and the expression of MLKL and ICAM-1 were estimated by real-time polymerase chain reaction at the mRNA level and Western blotting at the protein level. The adhesion of human monocyte cells (THP-1) to human umbilical vein endothelial cells (HUVECs) was examined under immunofluorescence microscopy, and the ability of cell adhesion was evaluated by ImageJ software. RESULTS Overexpression of MLKL greatly enhanced ICAM-1 expression in HUVECs and the adherence of THP-1 cells to HUVECs. Knockdown of MLKL by siRNA dramatically inhibited the expression of ICAM-1 and the adherence of THP-1 cells to HUVECs. MLKL could promote THP-1 adhesion to HUVECs by activating ICAM-1 expression in HUVECs. CONCLUSIONS MLKL can promote THP-1 cell adhesion to HUVECs through up-regulation of ICAM-1 expression in HUVECs. Thus, MLKL might be a useful target for reducing adhesion of monocytes to endothelial cells and atherosclerosis.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Quinases
/
Endotélio Vascular
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Monócitos
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Adesão Celular
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Regulação para Cima
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Molécula 1 de Adesão Intercelular
Limite:
Humans
Idioma:
En
Revista:
Med Sci Monit
Assunto da revista:
MEDICINA
Ano de publicação:
2020
Tipo de documento:
Article