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Endothelin-1 (ET-1) promotes a proinflammatory microglia phenotype in diabetic
Authors Abdul Y, Jamil S, He L, Li W, Ergul A
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal Canadian journal of physiology and pharmacology
Year 2020
Date Published 9/1/2020
Volume : Pages 98 : 596 - 603
PubMed Reference 32119570
Abstract Diabetes increases the risk and severity of cognitive impairment, especially
after ischemic stroke. It is also known that the activation of the endothelin
(ET) system is associated with cognitive impairment and microglia around the
periinfarct area produce ET-1. However, little is known about the effect of ET-1
on microglial polarization, especially under diabetic conditions. We
hypothesized that (i) ET-1 activates microglia to the proinflammatory M-1-like
phenotype and (ii) hypoxia/ lipopolysaccharide (LPS) activates the microglial ET
system and promotes microglial activation towards the M-1 phenotype in diabetic
conditions. Microglial cells (C8B4) cultured under normal-glucose (25 mmol/L)
conditions and diabetes-mimicking high-glucose (50 mmol/L) conditions for 48 h
were stimulated with ET-1, cobalt chloride (200 µmol/L), or LPS (100 ng/mL) for
24 h. PPET-1, ET receptor subtypes, and M1/M2 marker gene mRNA expression were
measured by RT-PCR. Secreted ET-1 was measured by ELISA. A high dose of ET-1 (1
µmol/L) increases the mRNA levels of ET receptors and activates the microglia
towards the M1 phenotype. Hypoxia or LPS activates the ET system in microglial
cells and shifts the microglia towards the M1 phenotype in diabetic conditions.
These in vitro observations warrant further investigation into the role of
ET-1-mediated activation of proinflammatory microglia in post-stroke cognitive
impairment in diabetes.


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