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MicroRNA-128b mediates lipopolysaccharide-induced apoptosis via reactive oxygen species in human pulmonary microvascular endothelial cells

OBJECTIVES: This study aimed to explore the effects of miR-128b in the regulation of Lipopolysaccharide (LPS) induced apoptosis. METHODS: Human Pulmonary Microvascular Endothelial Cells (HPMECs) were transfected with an miR-128b inhibitor and stimulated with LPS for 24 h. FCM was performed to detect...

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Detalles Bibliográficos
Autores principales: Long, Guangwen, Yang, Xiulin, Ji, Chunling, Dong, Yukang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hospital das Clinicas da Faculdade de Medicina da Universidade de Sao Paulo 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8933335/
https://www.ncbi.nlm.nih.gov/pubmed/35305480
http://dx.doi.org/10.1016/j.clinsp.2022.100020
Descripción
Sumario:OBJECTIVES: This study aimed to explore the effects of miR-128b in the regulation of Lipopolysaccharide (LPS) induced apoptosis. METHODS: Human Pulmonary Microvascular Endothelial Cells (HPMECs) were transfected with an miR-128b inhibitor and stimulated with LPS for 24 h. FCM was performed to detect apoptosis and Reactive Oxygen Species (ROS) production. In addition, miRNA and caspase-3 expression levels were determined using real-time quantitative polymerase chain reaction and western blotting. RESULTS: LPS significantly induced apoptosis and ROS production and upregulated miR-128b and caspase-3 expressions in HPMECs. However, LPS-induced effects were suppressed when an miR-128b inhibitor was used. Preincubation with NAC decreased the LPS-induced apoptosis of HPMECs. CONCLUSIONS: These effects were mediated by miR-128b via the caspase-3 pathway.