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Review
. 2015 Nov 1;4(11):623-630.
doi: 10.1089/wound.2014.0579.

The Role of Chemokines in Mesenchymal Stem Cell Homing to Wounds

Anne M Hocking  1
Affiliations
Review

The Role of Chemokines in Mesenchymal Stem Cell Homing to Wounds

Anne M Hocking. Adv Wound Care (New Rochelle). .

Abstract

Significance: Mesenchymal stem cells (MSCs) are being administered to cutaneous wounds with the goal of accelerating wound closure and promoting regeneration instead of scar formation. An ongoing challenge for cell-based therapies is achieving effective and optimal targeted delivery and engraftment at the site of injury. Contributing to this challenge is our incomplete understanding of endogenous MSC homing to sites of injury. Recent Advances: Chemokines and their receptors are now recognized as important mediators of stem cell homing. To date, the most studied chemokine-chemokine receptor axis in MSC homing to wounds is CXCL12-CXCR4 but recent work suggests that CCL27-CCR10 and CCL21-CCR7 may also be involved. Critical Issues: Strategies to enhance chemokine-mediated MSC homing to wounds are using a variety of approaches to amplify the chemokine signal at the wound site and/or overexpress specific chemokine receptors on the surface of the MSC. Future Directions: Harnessing chemokine signaling may enhance the therapeutic effects of stem cell therapy by increasing the number of both exogenous and endogenous stem cells recruited to the site of injury. Alternatively, chemokine-based therapies directly targeting endogenous stem cells may circumvent the need for the time-consuming and costly isolation and expansion of autologous stem cells prior to therapeutic administration.

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Figures

None
Anne M. Hocking, PhD
<b>Figure 1.</b>
Figure 1.
The minimal criteria for defining human bone marrow-derived MSC are: plastic adherence; positive for stromal markers and negative for hematopoietic markers; and capacity to differentiate in vitro into bone, fat, and cartilage. MSC, mesenchymal stem cell.
<b>Figure 2.</b>
Figure 2.
Structures of chemokines and their receptors. (A) Arrangement of four amino terminal cysteines in the CCL and CXCL families. (B) Chemokine receptors are G-protein-coupled receptors with seven transmembrane domains. Chemokines bind to the N-terminus of the receptor.
<b>Figure 3.</b>
Figure 3.
MSC homing to sites of injury involves chemotaxis. Chemokines released by wounds are immobilized on glycosaminoglycans on the endothelium. MSC migrate toward this gradient, adhere, and then transmigrate through the vessel wall into the wound.
<b>Figure 4.</b>
Figure 4.
Chemokine–chemokine receptor axes mediating stem cell homing to wounds. Homing of bone marrow-derived MSCs to wounds is mediated by the following chemokine–chemokine receptor axes: CXCL12-CXCR4, CCL27-CCR10, and CCL21-CCR4. Homing of EPC to wounds is mediated by CXCL12-CXCR4 and CCL5-CCR5. EPC, endothelial progenitor cells.
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