Topic: hypoxic injury

Identifying the mechanisms underlying the early stage of hypoxic injury of the retinocollicular neurotransmission will provide valuable insights that may be beneficial for the future intervening in visual attention and perception deficits and preventing their progressions. Previously, we have demonstrated that the protein kinase C (PKC) signaling pathway mediates hypoxia-induced LTP of NMDA retinocollicular neurotransmission. The potent and selective inhibitor of PKC - chelerythrine chloride (ChC, 5 µM) completely blocked the induction of LTP by hypoxia and even reversed already induced one. H

Hypoxic injury in developing glial cells and their differential response can result in neurological deficits in neonates. This study attempts to understand the role of autophagy in developing premyelinating oligodendrocytes (pre-OL), mature-OL and astrocytes exposed to hypoxic injury. Human fetal neural stem cell-derived pre-OL, mature OL and astrocytes were exposed to hypoxia (0.2% oxygen) and normoxia (20% oxygen) for 48 hours followed by RNA-sequencing. Transcriptomic analysis revealed upregulation of autophagy in mature OL and astrocytes but not in pre-OL. MO3.13 (resembling pre-OL) and SV

In preterm infants, hypoxic injury to premyelinating oligodendrocytes leads to failure of oligodendroglial maturation causing long-term neuromotor disabilities. As astrocytes influence oligodendrocyte maturation, this study aimed to analyze the transcriptomic changes in astrocytes after hypoxic injury, to identify possible pathways influencing myelination. Human fetal neural stem cell-derived astrocytes, expressing astrocyte-specific glial fibrillary-acidic protein (GFAP) and excitatory amino acid transporters (EAAT1 and EAAT2), were exposed to hypoxia (0.2% oxygen) and normoxia (20% oxygen) f

Oligodendrocyte (OL) development undergoes a maturation arrest when premyelinating OL prevalent in preterm fetuses, are exposed to hypoxic injury. Understanding molecular mechanisms controlling OL development may help develop therapeutic strategies in conditions like cerebral palsy. Human fetal neural stem cells (FNSCs) were differentiated into OL and transcriptional changes were analyzed (RNA sequencing). The JAK-STAT cell signaling pathway was implicated in terminal OL maturation. The MO3.13 cell line resembling premyelinating OL was differentiated into mature OL over 7 days, using phorbol 1