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Sir: We thank Dr. Lujan-Hernandez and colleagues for their insightful comments regarding our work examining the role of alternatively activated M2 macrophages in improving fat graft survival. Both our groups have observed the critical role played by the induction of angiogenesis following fat grafting, with greater vascular density associated with improved graft retention. The importance of angiogenesis has likewise been demonstrated by others.1,2 As Dr. Lujan-Hernandez et al. rightly point out, however, angiogenesis is unlikely to be the sole determinant of ultimate fat engraftment. Illustrative of this is the observation of Kølle et al. that grafts enriched ex vivo with adipose-derived stromal cells in human subjects demonstrated greater volume retention but no increase in vascular density 4 months after implantation.3 This finding would suggest that improvement in graft volume may also be highly dependent on adipogenesis, a point underscored by the work of Dr. Lujan-Hernandez and colleagues in which they have demonstrated increased adipogenesis in the setting of inflammation. On the whole, these observations point to a far more complex process involving an ever-shifting balance between angiogenesis and adipogenesis.4 In the current report, we failed to observe a difference in peroxisome proliferator-activated receptor-γ, a critical positive regulator of adipogenesis,5 after 3 days of culture in M2 macrophage-conditioned medium. Others have shown a similar failure of macrophage-conditioned medium to induce adipogenesis.6 We agree with Dr. Lujan-Hernandez et al. that our inability to detect a difference in peroxisome proliferator-activated receptor-γ expression at the time point assessed may be attributable to earlier induction of this gene. The other possibility is that soluble factors produced by M2 macrophages are inadequate on their own to trigger terminal maturation of preadipocytes. We are examining this very question through the use of co-cultures. Our early data suggest that endothelial precursor populations from the stromal vascular fraction serve as a robust source of proadipogenic factors. Although preliminary, this would point to a critical link between angiogenesis and adipogenesis. In conclusion, we would like to once more thank Dr. Lujan-Hernandez and colleagues for their valuable comments and discussion. DISCLOSURE The author has no financial interest to declare in relation to content of this communication. Michael Bezuhly, M.D. Izaak Walton Killam Health Centre 5850/5980 University Avenue P.O. Box 9700 Halifax, Nova Scotia B3K 6R8, Canada [email protected]

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