Arteriogenesis in murine adipose tissue is contingent on CD68(+)/CD206(+) macrophages

作者：Seaman Scott A; Cao Yiqi; Campbell Chris A; Peirce Shayn M^*

来源：Microcirculation, 2017, 24(4): e12341.

DOI：10.1111/micc.12341

• adipose
• arteriogenesis
• collateral vessel
• macrophage

ObjectiveThe surgical transfer of skin, fat, and/or muscle from a donor site to a recipient site within the same patient is a widely performed procedure in reconstructive surgeries. A surgical pretreatment strategy that is intended to increase perfusion in the flap, termed flap delay, is a commonly employed technique by plastic surgeons prior to flap transplantation. Here, we explored whether CD68(+)/CD206(+) macrophages are required for arteriogenesis within the flap by performing gain-of-function and loss-of-function studies in a previously published flap delay murine model.
Methods and ResultsLocal injection of M2-polarized macrophages into the flap resulted in an increase in collateral vessel diameter. Application of a thin biomaterial film loaded with a pharmacological agent (FTY720), which has been previously shown to recruit CD68(+)/CD206(+) macrophages to remodeling tissue, increased CD68(+)/CD206(+) cell recruitment and collateral vessel enlargement. Conversely, when local macrophage populations were depleted within the inguinal fat pad via clodronate liposome delivery, we observed fewer CD68(+) cells accompanied by diminished collateral vessel enlargement.
ConclusionsOur study underscores the importance of macrophages during microvascular adaptations that are induced by flap delay. These studies suggest a mechanism for a translatable therapeutic target that may be used to enhance the clinical flap delay procedure.

• 出版日期2017-5