Neurotrophin production in brain pericytes during hypoxia: A role of pericytes for neuroprotection

Extracellular Acidification Activates cAMP Responsive Element Binding Protein via Na+/H+ Exchanger Isoform 1–Mediated Ca 2+ Oscillation in Central Nervous System Pericytes

“…3,45,46 We have shown the neuroprotective roles of pericytes in brain ischemia. 47, 48 The present study demonstrated that PDGFR-β-positive cells accumulated in the peri-infarct area and encircled capillary lumens during the early phase of ischemia. Furthermore, we have found that several PDGFR-β-positive cells were colocalized with phosphorylated CREB and IL-6 at the early phase of ischemic insult and that the expression of IL-6 in the penumbra area tended to be reduced in the PDGFR-β+/− mice.…”

“…CREB in pericytes may contribute to angiogenesis, neurogenesis, and neuroprotection by initiating these processes after brain ischemia. 3,4,47,48 In the ischemic penumbra, the decrease in the glucose supply is mild in comparison with the oxygen supply. Because intracellular protons cause mitochondrial disorder, oxidative glucose metabolism is impaired.…”

Brain mesenchymal stem cells: The other stem cells of the brain?

“…neurons or indirectly via their immunomodulatory properties or the secretion of neurotrophins [74] . Consistent with this idea is the observation that pericytes migrate away from the vascular wall and could generate neurons in response to injury [75,76] .…”

Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity

“…NTRK1 and NTRK3 encode for tyrosine kinase receptors TrkA and TrkC, respectively. Nerve growth factor (NGF) preferentially binds to TrkA whereas neurotrophin-3 (NT3) binds at high affinity to TrkC to promote neuron survival and synaptic plasticity [Lamballe et al, 1991;Reichardt, 2006], including in hypoxic conditions [Lee et al, 2003;Lin et al, 2006;Ishitsuka et al, 2012]. TrkA is expressed in various neuronal populations including cholinergic neurons in the basal forebrain and striatum [Holtzman et al, 1995].…”