Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22.
Biochem Biophys Res Commun
; 509(2): 359-366, 2019 02 05.
Article
en En
| MEDLINE
| ID: mdl-30591217
ABSTRACT
Cell death and inflammation play critical roles in atherosclerosis. Pyroptosis, a novel proinflammatory programmed cell death process, participates in atherosclerosis pathogenesis. Recently, MALAT1 was identified as a pyroptosis-related long noncoding RNA (lncRNA). Here, we investigated the potential role and underlying mechanism of lncRNA MALAT1 in endothelial cells pyroptosis. We first established an endothelial cell pyroptosis model by stimulating EA.hy926 human endothelial cells (EA.hy926â¯cells) with high glucose. Then, we investigated lncRNA MALAT1 expression and found that it was upregulated in high glucose-treated EA.hy926â¯cells. Furthermore, lncRNA MALAT1 knockdown significantly inhibited high glucose-induced pyroptosis in EA.hy926â¯cells, which may critically influence atherosclerosis. Moreover, miR-22 was a target of lncRNA MALAT1 and was negatively correlated with lncRNA MALAT1. NLRP3 expression was significantly suppressed by transfection with a MALAT1-targeting antisense oligonucleotide (ASO). Ultimately, miR-22 overexpression abrogated the effect of MALAT1 on high glucose-induced EA.hy926â¯cells pyroptosis. Together, our results suggest that lncRNA MALAT1 promotes high glucose-induced pyroptosis of endothelial cells partly by affecting NLRP3 expression through competitively binding miR-22. Our findings indicate a new regulatory mechanism for endothelial cells pyroptosis under high-glucose stress, providing a novel therapeutic target for atherosclerosis.
Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
MicroARNs
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Células Endoteliales
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ARN Largo no Codificante
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Piroptosis
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Proteína con Dominio Pirina 3 de la Familia NLR
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Glucosa
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2019
Tipo del documento:
Article