Stem cell mechanism of action in neuroplasticity after stroke

Abstract

Stroke is the second leading cause of death in the world that may cause a permanent disability. In recent years, stem cell therapy for ischemic stroke has made great progress. Currently, there have been several studies on stem cell therapy in stroke that provide benefits for neuroplasticity using various cell sources and transplant procedures, but the mechanisms are still controversial. Therefore, the aim of this review was to analyze the various mechanisms of stem cells in enhancing neuroplasticity. Stem cell mechanism that increases neuroplasticity can be through various signaling pathways, namely the endothelin-3/EDNRB, SRY-related HMG-box 10 (SOX10), Wnt/β-Catenin, GF1R+ and C-X-C chemokine receptor type 4 (CXCR4) pathways, and through neurotrophic factor (NT-3), specialized extracellular matrix perineuronal net (ECM PNN), microRNA (miR-133b and Ex-miR-17-92+ cluster), as well as modulation of proteins namely phosphorylated collapsin response mediator protein 2 (CRMP2) and increased regulation of phosphorylated-cAMP response element-binding protein (p-CREB), growth associated protein 43 (GAP-43), and synaptophysin (SYP). In conclusion, various signaling pathways and other factors contribute in neuroplasticity increase due to stem cell therapy in stroke.