LAUSR

BACKGROUND The unpredictable and unstable tissue retention rate of autologous fat grafting remains an obstacle faced by plastic surgeons. Our previous study using fat grafting mice model with donor site showed ASCs infiltration in recipient site was delayed, leading to poor regeneration and lower retention. Thus, the mechanism behind the differential infiltration of ASCs required to be explored. METHODS Firstly, we locally injected CXCL12 or CXCR4 inhibitor AMD3100 in recipient or donor site respectively (CXCL12+AMD3100-Group, CXCL12-AMD3100+Group, and CXCL12+AMD3100+Group). We compared the migration of ASCs, adipose regeneration and long-term retention. Next, we explored the role of angiogenesis using a Normal/Ischemic mice model in which we test the expression of CXCL12/CXCR4, migration of ASCs, and adipose regeneration. RESULTS Blocking CXCL12 in donor site using AMD3100 (CXCL12-AMD3100+, and CXCL12+AMD3100+Group) could accelerate ASCs infiltration, promote adipose regeneration and long-term retention (p<0.05) compared with the other groups. CXCL12 and its receptor CXCR4 expressed higher in Normal than in Ischemic adipose tissue; consistently, there were more ASCs infiltrating Normal than Ischemic adipose tissue early after surgery (p<0.05). CONCLUSION Early angiogenesis is essential for CXCL12 in promoting ASCs infiltration, improving adipose tissue repair in recipient site and potentiating long-term fat retention rate.