Harnessing Macrophages for Vascularization in Tissue Engineering
In this review, we explore the roles of macrophages both in vessel development and in vascularization of tissue engineered constructs. Upon the implantation of tissue engineered constructs into the body, macrophages respond, invade and orchestrate the host’s immune response. By altering their phenotype, macrophages can adopt a variety of roles. They can promote inflammation at the site of the implanted construct; they can also promote tissue repair. Macrophages support tissue repair by promoting angiogenesis through the secretion of pro-angiogenic cytokines and by behaving as support cells for nascent vasculature. Thus, the ability to manipulate the macrophage phenotype may yield macrophages capable of supporting vessel development. Moreover, macrophages are an easily isolated autologous cell source. For the generation of vascularized constructs outside of the body, these isolated macrophages can also be skewed to adopt a pro-angiogenic phenotype and enhance blood vessel development in the presence of endothelial cells. To assess the influence of macrophages on vessel development, both in vivo and in vitro models have been developed. Additionally, several groups have demonstrated the pro-angiogenic roles of macrophages in vascularization of tissue engineered constructs through the manipulation of macrophage phenotypes. This review comments on the roles of macrophages in promoting vascularization within these contexts.
KeywordsMacrophages Vascularization Vessel development Macrophage phenotypes Tissue engineering
The authors would like to acknowledge Chih-Wei Hsu for the use of his image (Fig. 5). The authors would also like to thank Dr. Botchwey for the use of Fig. 4: Reprinted from Ref. 29. Figure 3, Reprinted from Ref. 39. Funding was provided by National Science Foundation (Grant No. DGE-1644868), Foundation for the National Institutes of Health (Grant No. R01 HL097520).
Conflict of interest
The authors declare no conflicts of interest with regards to this manuscript.
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