Topic: HIF-1α

Microglia activation is a metabolically demanding process that implies the transition to a pro- or anti-inflammatory phenotype. During inflammation, microglia undergo metabolic reprogramming to meet their energy needs. Thus, the pro-inflammatory phenotype derives its energy mainly from aerobic glycolysis, whereas the anti-inflammatory phenotype depends on oxidative phosphorylation. The modulation of metabolic pathways in activated microglia could change their phenotype. Exogenously administered agmatine pretreatment (Agm, 100 µM) modulates the Lps-activated BV-2 microglial cell line towards an

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

Metabolic regulation in the nervous system plays a pivotal role in orchestrating neuronal function and maintaining cellular homeostasis. Utilizing our RNAseq data from gain- and loss-of-function studies of embryonic neural tissue and neuronal cells, we demonstrate that the nuclear receptor NR5A2 regulates hypoxia response, glycolysis, and fatty acid metabolism. Consistently, we have previously shown that NR5A2 inhibits the proliferation and growth of glioblastoma cells and tumors, respectively. Here, we elucidate a novel mechanism whereby NR5A2 functions as a potent suppressor of HIF-1α (Hypox

Ischemic stroke results in neuroinflammation. While several studies addressed its molecular mechanism, we know less about the contribution of physical cues to stroke pathomechanism. In the present work, we aimed to address the significance of nervous tissue cytoskeleton rearrangements and changes in its mechanical properties in neuroinflammation. We applied oxygen-glucose deprivation (OGD) on rat organotypic hippocampal cultures (OHCs) as our model of brain ischemia. We observed that OGD significantly increases LHD and NO release from OHCs. HIF-1α protein expression was also significantly incr