Skin wound healing involves highly complex coordinated interactions of different cell types, tissues, and biochemical mediators. It is usually accompanied by a transient increase in blood vessel permeability, due to the enlargement of cell junction gaps modulated by inflammatory mediators after injury. Vascular barrier integrity will be re‐established through restoration of tight junctions by recruiting supporting cells and producing extracellular matrix for stabilization of the vessels in and around the wounded area. Granulocyte macrophage colony stimulating factor (GM‐CSF) with pleiotropic functions enhances wound healing via recruiting inflammatory cells, stimulating reepithelization and angiogenesis. Our previous report demonstrated that wound healing is compromised in GM‐CSF KO mice, accompanied with reduced infiltration of neutrophils and macrophages. Furthermore, insufficient vascularization is observed in the wound beds of GM‐CSF KO mice. As expected, wound healing is enhanced with exogenous GM‐CSF, particularly in patients with diabetes or hydroxyurea‐related leg ulcers. Therefore, it is believed that GM‐CSF plays a key role during wound healing via promotion of angiogenesis in wound beds. Besides, it is reported GM‐CSF regulates maturation of microvessels by manipulating the spatial‐temporal Ang‐1/Ang‐2 balance and the phosphorylation of Tie‐2. The results of studies provide a strong rationale for the exploration of GM‐CSF in vessel
Wound Repair and Regeneration – Wiley
Published: Jan 1, 2017
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