Open AccessConcise Review: The Potential of Stromal Cell‐Derived Factor 1 and Its Receptors to Promote Stem Cell Functions in Spinal Cord Repair
Author(s) -
Jaerve Anne,
Schira Jessica,
Müller Hans Werner
Publication year - 2012
Publication title -
stem cells translational medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.781
H-Index - 71
eISSN - 2157-6580
pISSN - 2157-6564
DOI - 10.5966/sctm.2012-0068
Subject(s) - stem cell , stromal cell , progenitor cell , cxcr4 , microbiology and biotechnology , spinal cord injury , biology , regeneration (biology) , stem cell factor , stem cell therapy , neural stem cell , adult stem cell , immunology , neuroscience , cellular differentiation , chemokine , cancer research , spinal cord , inflammation , biochemistry , gene
Transplanted stem cells provide beneficial effects on regeneration/recovery after spinal cord injury (SCI) by the release of growth‐promoting factors, increased tissue preservation, and provision of a permissive environment for axon regeneration. A rise in chemokine stromal cell‐derived factor 1 (SDF‐1/CXCL12) expression levels in central nervous system (CNS) injury sites has been shown to play a central role in recruiting transplanted stem cells. Although technically more challenging, it has been shown that after SCI few endogenous stem cells are recruited via SDF‐1/CXCR4 signaling. Evidence is accumulating that increasing SDF‐1 levels at the injury site (e.g., by exogenous application or transfection methods) further enhances stem cell recruitment. Moreover, SDF‐1 might, in addition to migration, also influence survival, proliferation, differentiation, and cytokine secretion of stem cells. Here, we discuss the experimental data available on the role of SDF‐1 in stem and progenitor cell biology following CNS injury and suggest strategies for how manipulation of the SDF‐1 system could facilitate stem cell‐based therapeutic approaches in SCI. In addition, we discuss challenges such as how to circumvent off‐target effects in order to facilitate the transfer of SDF‐1 to the clinic.