Transplant immunology · 2021
MiR-702-3p inhibits the inflammatory injury in septic H9c2 cells by regulating NOD1.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Chun, Yang Yang, Liang Guiwen, Zhang Aixian, Xu Feng
Аннотация
BACKGROUND: Cardiac insufficiency is a common complication of sepsis and septic shock and is the most common cause of death in critically ill patients. Recent studies have found that microRNAs (miRNAs) play a potential role in sepsis as markers, but little is known about their functional effects on sepsis-induced cardiomyopathy (SIC).
OBJECTIVE: This study is designed to explore the possible role and underlying mechanisms of miR-702-3p in septic cardiomyopathy.
METHODS: As expected, H9c2 cells were induced with lipopolysaccharide (LPS) to construct the model of septic cardiomyopathy. The expression of miR-702-3p was detected by qRT-PCR assay and those of IL-1β, IL-6 and TNF-α by ELISA assay. The viability, proliferation and apoptosis of LPS-treated H9c2 cells were determined by CCK-8, EdU, flow cytometry and western blot assays. Moreover, Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) was predicted and confirmed as a direct target of miR-702-3p by TargetScan, miRwalk and miRDB prediction and dual-luciferase reporter gene assays.
RESULTS: While LPS can weaken the viability of H9c2 cells, miR-702-3p enhances that of LPS-treated H9c2 cells by inhibit the expressions of TNF-α, IL-6, IL-1β. We found NOD1 is a target gene of miR-702-3p, and over-expression of NOD1 restores the inhibitory effects of miR-702-3p on the LPS-treated H9c2 cells.
CONCLUSION: MiR-702-3p played an important role in the pathogenesis of sepsis cardiomyopathy via targeting NOD1, suggesting that miR-702-3p may be a potential new target for the treatment of SIC.
OBJECTIVE: This study is designed to explore the possible role and underlying mechanisms of miR-702-3p in septic cardiomyopathy.
METHODS: As expected, H9c2 cells were induced with lipopolysaccharide (LPS) to construct the model of septic cardiomyopathy. The expression of miR-702-3p was detected by qRT-PCR assay and those of IL-1β, IL-6 and TNF-α by ELISA assay. The viability, proliferation and apoptosis of LPS-treated H9c2 cells were determined by CCK-8, EdU, flow cytometry and western blot assays. Moreover, Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) was predicted and confirmed as a direct target of miR-702-3p by TargetScan, miRwalk and miRDB prediction and dual-luciferase reporter gene assays.
RESULTS: While LPS can weaken the viability of H9c2 cells, miR-702-3p enhances that of LPS-treated H9c2 cells by inhibit the expressions of TNF-α, IL-6, IL-1β. We found NOD1 is a target gene of miR-702-3p, and over-expression of NOD1 restores the inhibitory effects of miR-702-3p on the LPS-treated H9c2 cells.
CONCLUSION: MiR-702-3p played an important role in the pathogenesis of sepsis cardiomyopathy via targeting NOD1, suggesting that miR-702-3p may be a potential new target for the treatment of SIC.