GSE123829
Autologous microgratf accelerates endogenous wound healing response through ERK-induced cell migration.
Defective fibroblast migration cause delayed wound healing (WH) and chronic skin lesions. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of WH-associated growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn leads to increased cell migration rate by elevating activity of ERK and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Moreover, AMG-treated wounds showed increased granulation tissue formation and organized collagen content. Overall, we shed light on AMG molecular mechanism supporting its potential to trigger highly improved wound healing process. Overall design: A total of 14 samples have been used to analyse transcriptome changes in wounded murine primary fibroblasts upon Autologous Micrograft (AMG) treatment. Samples have been divided in two groups: Untreated and AMG-treated. Samples have been exposed to AMG treatment for different time periods (1, 5, 12 and 24 hours). Each time of treatment includes 1 biological sample, except for 5 hours of treatment where we included three additional biological replicates.