17β-estradiol suppresses hyperoxia-induced apoptosis of oligodendrocytes through paired-immunoglobulin-like receptor B

Abstract

Hyperoxia is a high risk factor for neurodevelopmental disorders and can cause nerve cell death. 17β‑Estradiol (E2) has been demonstrated as a neuroprotective agent. In the present study, the effect of hyperoxia on rat oligodendrocyte precursor cells (OPCs) in vivo and the neuroprotective effects of E2 on these cells were investigated. OPCs were treated with various concentrations of E2 and were harvested for reverse transcription‑quantitiative polymerase chain reaction (RT‑qPCR) analysis at various time‑points. RT‑qPCR analysis demonstrated that paired immunoglobin‑like receptor B (PriB) PriB mRNA expression levels were markedly decreased following treatment with 10(‑6), 10(‑7) and 10(‑8) M E2. Cells treated with 10(‑7) M E2 for 24 h were selected for subsequent experiments. PriB was silenced with small interfering (si)RNA and the effects of E2 treatment and silencing of PriB on the viability and apoptosis of OPCs under hyperoxic stimulation was detected using 3‑(4,5‑dimethyl‑2‑thiazolyl)‑2,5‑diphenyl‑2‑H‑tetrazoliu‑bromide (MTT) assay and flow cytometry analysis. The results revealed that hyperoxia induced apoptosis in OPCs and decreased their viability. Hyperoxia also induced the expression of caspases‑3 and ‑8, and Fas cell surface death receptor (Fas). E2 treatment markedly downregulated the expression of PirB. E2 treatment or PirB silencing markedly decreased hyperoxia‑induced apoptosis, increased cell viability and decreased the expression of caspases‑3 and ‑8, and Fas in OPCs, indicating that E2 protects OPCs from hyperoxia‑induced apoptosis, predominantly through the downregulation of PirB The results of the present study provide a theoretical basis for the reasonable use of oxygen in Neonatal Intensive Care Units.

Mechanistic advances of hyperoxia-induced immature brain injury

“… Years O 2 (%) Duration Cell Outcome Ref 2006 80 24–96 h OLN-93 OPCs apoptosis [ 27 ] 2008 80 0–24 h OPCs OPCs apoptosis [ 28 ] 2012 80 24 h OPCs and microglia OPCs death [ 32 ] 2014 80 24 h OPCs OPCs death [ 40 ] 2015 80 ? Astrocytes PDGFA reduction, and hypomyelination [ 41 ] 2016 80 24 h OPCs OLs degeneration and maturation impaired [ 44 ] 2016 80 24 h OPCs OPCs apoptosis [ 72 ] 2019 80 24 h OPCs, microglia and astrocytes PDGFA improved OPCs proliferation and myelination [ 56 ] 2020 80 24 h OPCs ...…”

“…E2, a form of the estrogen hormone, has neuroprotective properties in hyperoxia induced in vitro. E2 protects OPCs from hyperoxia-induced apoptosis by downregulating paired immunoglobulin-like receptor B [ 72 ] and preventing their migration [ 95 ], thereby reducing microglial activation and oxidative stress [ 19 ]. These properties result from the activation of E2 receptors and crosstalk with intracellular signaling pathways [ 138 ].…”

Subtle side chain modification of triphenylamine‐based polymer hole‐transport layer materials produces efficient and stable inverted perovskite solar cells

“…Triphenylamine derivatives PTAA and Poly-TPD are the most widely adopted polymer HTMs in IPVSCs, due to their favorable energy levels, lower annealing temperatures, and intrinsic hydrophobicity. [18][19][20][21] Poly-TPD and PTAA also exhibit perovskite passivation effects [22,23] ; however, the exact mechanism (i.e., the functional group responsible for passivation) is still unclear, which hinders the further development of these materials.…”