Last Updated: 20/11/2024
Mast cell exosomes mediate miR-27a targeting endoplasmic reticulum stress IRE1 regulates the mechanism of brain malaria neuron injury
Objectives
The central hypothesis is that mast cells degranulation can aggravate the pathogenesis of neuronal damage in CM through the secretion of exosomes. This project will use murine CM model, mast cells and neuron in vitro experiments, test that, 1) exosomal miR-27a secreted form mast cells can participate in cross-talk among brain mast cells and neurons, 2) exosomal miR-27a secreted form mast cells can aggravate the pathogenesis of neuronal damage in CM through targeting endoplasmic reticulum stress-IRE1 signaling pathway.
Qi Wang
Wanting Wu
Mingqiang Li
Fei Tuo
Guanghui Zhao
Yuan-Liang Liu
Long-term neurological impairments are frequently detected in surviving cerebral malaria (CM) patients. The pathophysiology and therapy of long lasting cognitive deficits in CM patients after treatment of the parasitic disease is a critical area of investigation, which is called for exploring the mechanism of neuronal damage in CM. It was reported that mast cells modulated function and behavior of brain. The preliminary data showed that, both the numbers and degranulated percentage of mass cells were significantly increased in the brain tissue of experimental CM; activation of mast cells by Compound 48/80 intracerebroventricular injection resulted in enhanced neuronal apoptosis, p-IRE1 (that is related to endoplasmic reticulum stress-induced apoptosis), and exosome in the brain tissue of experimental CM; the elevated expression of miR-27a was also observed on the exosomes secreted form activation of mast cells in vitro. It was reported that cross-talk was among brain mast cells and neurons through exosomal microRNAs. The findings will provide new treatment ideas and new adjuvant drugs for the therapies of CM disease.
Jan 2018 — Dec 2020
$29,380
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