Research Information System
45th FEBS Congress, “Molecules of Life: Towards New Horizons“,, Ljubljana, Slovenia, 3 - 08 July 2021, pp.146, (Summary Text)
Abnormal wound healing can cause keloid scar formation. Keloids are fibrous benign tumours that continue growing beyond the wound boundaries. It is characterized
by increased collagen accumulation. Therefore, targeting collagen synthesis may be the right approach for treatment. Evidence is emerging regarding the efficacy of the
miR29 family in fibrotic diseases and extracellular matrix proteins are dominant among target molecules. In this study, we examined the role of miR29 family in keloids,
HSP47 and LOX for collagen maturation and collagen synthesis through the TGFb/
Smad pathway. We determined the skin keloid and control tissue miR29 family
gene levels via qPCR. After determining miR29 expressions in keloid scar tissues, we inhibited miR29a in primary keloid fibroblasts. We checked the protein levels
related to collagen synthesis by using western blotting. TGFb/
Smad pathway gene levels were determined by using qPCR. Extracellular LOX activity was measured
with a fluorescent kit, and TIMP1
protein levels were assessed with ELISA. As a result, it has been found a significant increase in fibronectin, COL1A and LOXL2
protein levels, and LOX activity. These parameters proved that miR29a affects the collagen synthesis process and increases collagen synthesis. On the other hand, the
downregulation of miR29a in keloids increased TGFb/
Smad pathway activity. TIMP1
gene levels upregulated with this activity, but this was not reflected in the
extracellular TIMP1
protein level. This may indicate that miR29a affects TGFb,
TGFb
stimulates TIMP1,
but this stimulation may not be reflected in the protein
level of TIMP1
and may be a cause of the irregularity in keloid histopathology. These findings indicate that miR29a is effective in keloid formation and this activity is
related to the expression level of miR29a.