MicroRNA-144-3p enhances LPS induced septic acute lung injury in mice through downregulating Caveolin-2.
Immunol Lett
; 231: 18-25, 2021 03.
Article
en En
| MEDLINE
| ID: mdl-33418009
ABSTRACT
OBJECTIVE:
The emphasis of this study focused on the possible implication and the mechanism of miR-144-3p in septic acute lung injury (ALI) condition.METHODS:
Mice were pre-injected with miR-144-3p agomir, miR-144-3p antagomir, sh-Caveolin-2 or PBS before 10 mg/kg LPS induced sepsis model establishment. The ratio of wet weight of lung tissues and body weight (W/W) was calculated. The pathological changes on lung tissues were observed by H&E staining. Secretions of inflammatory cytokines (TNF-α, IL-1ß and IL-6) in both mouse serum and lung tissues were determined by ELISA. Cell apoptosis and cell morphology were measured by TUNEL staining and H&E staining. The expressions of miR-144-3p, Caveolin-2, apoptotic related proteins and JAK/STAT pathway related proteins were measured by qRT-PCR or/and Western blot. Dual luciferase reporter assay was applied to detect the binding of miR-144-3p with Caveolin-2.RESULTS:
LPS resulted in increased W/W, disrupted lung tissue, enhanced inflammatory response and cell apoptosis. miR-144-3p was upregulated while Caveolin-2 was downregulated in response to LPS treatment. Inflammation and cell apoptosis induced by LPS can be alleviated by miR-144-3p antagomir injection, but enhanced by miR-144-3p agomir or sh-Caveolin-2 treatment. miR-144-3p can negatively target Caveolin-2. miR-144-3p can activate the JAK/STAT signal pathway through Caveolin-2 in septic ALI mouse.CONCLUSION:
miR-144-3 can promote LPS induced septic ALI through downregulating Caveolin-2 to activate the JAK/STAT signal pathway.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Regulación de la Expresión Génica
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Sepsis
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MicroARNs
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Interferencia de ARN
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Susceptibilidad a Enfermedades
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Caveolina 2
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Immunol Lett
Año:
2021
Tipo del documento:
Article