17β‑estradiol suppresses hyperoxia‑induced apoptosis of oligodendrocyte precursor cells through paired‑immunoglobulin‑like receptor B.
- Author:
Hua WANG
1
;
De-Zhi MU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Estradiol; pharmacology; Hyperoxia; pathology; Neuroprotective Agents; pharmacology; Oligodendroglia; drug effects; physiology; Rats; Rats, Sprague-Dawley; Receptors, Immunologic; physiology; Stem Cells; drug effects; physiology
- From: Chinese Journal of Contemporary Pediatrics 2016;18(7):650-655
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of hyperoxia and paired immunoglobin-like receptor B (PirB) on rat oligodendrocyte precursor cells (OPCs) in vivo and the neuroprotective effects of 17β-estradiol (E2) on these cells.
METHODSRat OPCs were treated with different concentrations of E2 and the cells were harvested for RT‑qPCR analysis at different time points. PriB was silenced with small interfering siRNA. The effects of E2 treatment and silencing of PriB on OPCs viability and apoptosis under hyperoxic stimulation were detected using 3‑(4,5‑dimethylthi‑azol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis.
RESULTSHyperoxia induced apoptosis in OPCs and decreased their viability. E2 treatment markedly down-regulated the expression of PirB. E2 treatment or PirB silencing markedly decreased hyperoxia-induced apoptosis and increased cell viability in OPCs.
CONCLUSIONSE2 can protect OPCs from hyperoxia-induced apoptosis.
