The impact of hypoxic-ischemic brain injury on stem cell mobilization, migration, adhesion, and proliferation

Abstract

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.

Keywords

• brain-derived neurotrophic; hypoxia inducible; erythropoietin; factor; matrix metalloproteinase; neonatal; stromal cell-derived; vascular endothelial growth