In-vitro functional experiments showed hsa-miR31-5p knockdown remarkably suppressed the proliferation of hypertrophic scar fibroblasts (HSFBs) under hypoxia, promoted cell invasion, and inhibited the expression of Collagen I and III and Fibronectin (FN), suggesting that hsa-miR31-5p knockdown effectively reduces HS formation caused by excessive ECM synthesis and deposition in HSFBs under hypoxia.
Immunohistochemistry was performed to examine the expression levels of laminin, fibronectin (FN), collagen type I (Col1) and HOXB9 in hypertrophic scar and healthy skin tissues, and in lentivirus‑constructed HOXB9‑overexpressed or ‑silenced fibroblasts (FBs).
We recently demonstrated that the accumulation of extracellular matrix in post-burn hypertrophic scarring (HSc) tissues is, in part, caused by an overexpression of mRNA for fibronectin, type I, and type III procollagen.