Investigation of the presence of mir-29 family, effect of mir-29 on collagen maturation and role in signaling pathways related to extracellular matrix synthesis in fibro-proliferative scars

Abnormal wound healing can cause fibroproliferative scar formation. These are hypertrophic scarring and keloids. Hypertrophic scar is a fibrotic pathology that continues to grow in the wound. Keloids are fibrous benign tumors that continue to grow beyond the wound boundaries. The mechanisms of both pathological conditions are still not fully elucidated. They are characterized by increased collagen deposition. Therefore, targeting collagen synthesis may be the right approach for treatment. Evidence is emerging for the efficacy of the miR29 family in fibrotic diseases, and extracellular matrix proteins predominate among target molecules. In this study, we examined the role of miR29 family in fibroproliferative scars, the role of HSP47 and LOX in collagen maturation and collagen synthesis by TGF-/ Smad pathway. After determining miR29 expressions in fibroproliferative scar and healthy control skin tissues, we inhibited miR29 in fibroproliferative scar and skin fibroblasts and found a significant increase in COL1A after suppression in keloid fibroblasts, and in COL3A and HSP47 protein levels in hypertrophic scars. The TGF-/ Smad signaling pathway was also activated by the suppression of miR29. While TIMP-1 gene and protein levels increased in hypertrophic scar, TIMP-1 gene expression increased and protein level decreased in keloid. These findings show that miR29 is effective in fibroproliferative scar formation and this activity is related to the level of miR29 expression.