Paralemmin-3 augments lipopolysaccharide-induced acute lung injury with M1 macrophage polarization via the notch signaling pathway.
Respir Physiol Neurobiol
; 320: 104203, 2024 Feb.
Article
en En
| MEDLINE
| ID: mdl-38103708
ABSTRACT
BACKGROUND:
Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action.METHODS:
An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization.RESULTS:
PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling.CONCLUSION:
PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments.Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Lipopolisacáridos
/
Lesión Pulmonar Aguda
Límite:
Animals
Idioma:
En
Revista:
Respir Physiol Neurobiol
Año:
2024
Tipo del documento:
Article