LncRNA MALAT1 promotes high glucose-induced inflammatory response of microglial cells via provoking MyD88/IRAK1/TRAF6 signaling

Scientific Reports
Li-Qing Wang, Heng-Jun Zhou

Abstract

Although a large number of studies have confirmed from multiple levels that diabetes mellitus (DM) promotes cerebral ischemic reperfusion (I/R) injury, but the precise mechanism is still unclear. A cerebral I/R injury model in diabetic rats was established. The neurological deficit scores and brain edema were monitored at 24 and 72 hours after injury. The peri-infarct cortical tissues of rats were isolated for molecular biology detection. The rat primary microglia and microglia line HAPI were cultured to establish the cell model of DM-I/R by high glucose (HG) and hypoxia-reoxygenation (H/R). The endogenous expression of MALAT1 and MyD88 was regulated by the transfection with pcDNA-MALAT1, si-MALAT1 and si-MyD88, respectively. The cerebral I/R injury model in diabetic rats had more severe neuronal injury as shown by the significantly higher neurological deficit scores and an obvious increasing brain edema at 24 and 72 hours after injury. Moreover, the microglia were activated and induced a large number of inflammatory cytokines TNF-α, IL-1β and IL-6 in the peri-infarct cortical tissues during cerebral I/R injury associated with DM. The expression of MALAT1, MyD88, IRAK1 and TRAF6 protein were significantly up-regulated by DM-I/R...Continue Reading

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Citations

May 17, 2019·Clinical Epigenetics·Simin Tang HanbingWang
Dec 20, 2019·IUBMB Life·Youyou YanChunli Song
Jan 6, 2019·Journal of Molecular Neuroscience : MN·Jalal GharesouranMir Davood Omrani

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Methods Mentioned

BETA
ELISA
PCR
transfection
immunoprecipitation
flow cytometry
histone acetylation

Software Mentioned

SPSS
Gel imaging system
AUTOCAD2000
Longa

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