Photothermal lipolysis accelerates ECM production via macrophage-derived ALOX15-mediated p38 MAPK activation in fibroblasts.

Skin and subcutaneous tissue tightening is usually treated by noninvasive photothermal treatment for medical aesthetics purpose, while the underlying mechanism remains to be elucidated. Here we hypothesized that adipocyte injury, as a stimulator, may regulate ECM production by increasing ALOX15 in macrophages, which could lead to fibroblast activation. In this study, we show that lipolysis was induced by laser heating (45°C for 15 minutes) in patients and rats, and adipocyte thermal injury stimulates the ECM production in fibroblasts by ALOX15 that was increased in co-cultured macrophages. These phenomena were evidenced by the ALOX15 knockdown. In addition, ALOX15 metabolite 12(S)-HETE activated p38 MAPK signaling pathway that mediated the production of ECM in fibroblast. In summary, the results of this study demonstrate that the mechanisms of adipose photothermal injury-induced skin and/or subcutaneous tissue tightening may have clinical relevance for noninvasive or minimally invasive photothermal therapeutics. This article is protected by copyright. All rights reserved.