Open AccessThe impact of hypoxic-ischemic brain injury on stem cell mobilization, migration, adhesion, and proliferation
Author(s) -
Stephanie M Parry,
Eric S. Peeples
Publication year - 2018
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.235012
Subject(s) - medicine , stem cell , hypoxic ischemic encephalopathy , stem cell therapy , transplantation , encephalopathy , hypothermia , brain damage , neuroscience , hypoxia (environmental) , bioinformatics , microbiology and biotechnology , biology , chemistry , organic chemistry , oxygen
Neonatal hypoxic-ischemic encephalopathy continues to be a significant cause of death or neurodevelopmental delays despite standard use of therapeutic hypothermia. The use of stem cell transplantation has recently emerged as a promising supplemental therapy to further improve the outcomes of infants with hypoxic-ischemic encephalopathy. After the injury, the brain releases several chemical mediators, many of which communicate directly with stem cells to encourage mobilization, migration, cell adhesion and differentiation. This manuscript reviews the biomarkers that are released from the injured brain and their interactions with stem cells, providing insight regarding how their upregulation could improve stem cell therapy by maximizing cell delivery to the injured tissue.