scholarly journals Human Umbilical Cord Therapy Improves Long-Term Behavioral Outcomes Following Neonatal Hypoxic Ischemic Brain Injury

2019 ◽  
Vol 10 ◽  
Author(s):  
Tayla R. Penny ◽  
Amy E. Sutherland ◽  
Jamie G. Mihelakis ◽  
Madison C. B. Paton ◽  
Yen Pham ◽  
...  
Keyword(s):  
Brain Injury ◽  
Umbilical Cord ◽  
Behavioral Outcomes ◽  
Human Umbilical Cord ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals 364: Neuroregenerative functions of transnasal delivered umbilical cord stem cells in a model of preterm hypoxic-ischemic brain injury

2016 ◽  
Vol 214 (1) ◽  
pp. S203-S204
Author(s):  
Byron Oppliger ◽  
Marianne Jörger-Messerli ◽  
Martin Müller ◽  
Ursula Reinhart ◽  
Philipp Schneider ◽  
...  
Keyword(s):  
Stem Cells ◽  
Brain Injury ◽  
Umbilical Cord ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Umbilical Cord Stem Cells ◽  
Hypoxic Ischemic Brain Injury

scholarly journals C3a Receptor Signaling Inhibits Neurodegeneration Induced by Neonatal Hypoxic-Ischemic Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea Pozo-Rodrigálvarez ◽  
YiXian Li ◽  
Anna Stokowska ◽  
Jingyun Wu ◽  
Verena Dehm ◽  
...  
Keyword(s):  
Brain Injury ◽  
Perinatal Asphyxia ◽  
Brain Inflammation ◽  
Biologically Active ◽  
Reactive Gliosis ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Transgenic Expression ◽  
Hypoxic Ischemic Brain Injury

Hypoxic-ischemic neonatal encephalopathy due to perinatal asphyxia is the leading cause of brain injury in newborns. Clinical data suggest that brain inflammation induced by perinatal insults can persist for years. We previously showed that signaling through the receptor for complement peptide C3a (C3aR) protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. We found that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting 1 h after induction of hypoxia-ischemia reduced neurodegeneration and reactive gliosis in the hippocampus of wildtype mice. We conclude that neonatal hypoxic-ischemic brain injury leads to long-lasting neurodegeneration. This neurodegeneration is substantially reduced by treatment with C3aR agonists, conceivably through modulation of reactive gliosis.

Optimization of behavioral testing in a long-term rat model of hypoxic ischemic brain injury

2021 ◽  
Vol 409 ◽  
pp. 113322
Author(s):  
Tayla R. Penny ◽  
Yen Pham ◽  
Amy E. Sutherland ◽  
Madeleine J. Smith ◽  
Joohyung Lee ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Ischemic Brain Injury ◽  
Behavioral Testing ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury
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