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Down-regulation of miR-133a-3p protects lung tissue against sepsis-induced acute respiratory distress syndrome by up-regulating SIRT1.
Hui, Qin; Zhang, Qi; Li, Xuan; Wang, Kundi; Zhang, Jing; Zhou, Zhongshu.
Afiliación
  • Hui Q; Department of Pediatrics, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
  • Zhang Q; Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
  • Li X; Department of Pediatrics, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
  • Wang K; Department of Pediatrics, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
  • Zhang J; Department of Pediatrics, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
  • Zhou Z; Department of Pediatrics, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
Arch Med Sci ; 20(1): 289-301, 2024.
Article en En | MEDLINE | ID: mdl-38414466
ABSTRACT

Introduction:

MicroRNA-133a-3p (miR-133a-3p) is a potential gene regulator having an important role in the process of inflammation and lung injury. The present work studied the role of miR-133a-3p in sepsis-mediated acute respiratory distress syndrome (ARDS) and the mechanism involved. Material and

methods:

C57BL/6 mice were selected for the study. Protein expression of Bcl-2, cleaved caspase-3 and Bax was assessed by western blot analysis. Expression of mRNA was assessed by RT-PCR. Effects of inflammation were studied by myeloperoxidase (MPO) activity. Quantification of albumin was done by measuring the albumin conjugated with Evan's blue. The alveolar macrophages were separated from the lungs of mice by the bronchoalveolar lavage procedure and were submitted to sepsis challenge in vitro; the macrophages were treated with lipopolysaccharide (LPS).

Results:

Treatment of LPS resulted in upregulation of miR-133a-3p in alveolar macrophages. Suppression of miR-133a-3p halted the over-expression of inflammatory cytokines in macrophages and caused remission of histopathologic changes. The ARDS lungs showed a decrease in levels of proinflammatory cytokines and an increase in levels of apoptotic protein, establishing the protective role for miR-133a-3p. The results suggested sirtuin 1 (SIRT1) as a potential target of miR-133a-3p in the macrophages, also showing that expression of SIRT1 was inversely associated with expression of miR-133a-3p. The protective effect of miR-133a-3p down-regulation in LPS-mediated alveolar macrophages and sepsis-induced ARDS could be corrected by a SIRT1 inhibitor.

Conclusions:

Down-regulation of miR-133a-3p may exert a protective effect on lung tissue against sepsis-mediated ARDS by up-regulating the levels of SIRT1 via suppressing the inflammatory response and inhibiting the cellular apoptosis in lung tissues.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Arch Med Sci Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Polonia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Arch Med Sci Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Polonia