Assessing the mechanisms of defective TGF-β1 response in chronic wound fibroblasts


During chronic kidney disease (CKD), increased expression of TGF-β1 results in the excessive accumulation of extracellular matrix (ECM) proteins and intracellular α-smooth muscle actin (αSMA) fibres. This results in renal fibrosis and loss of renal function. Fibroblast cells differentiate into contractile myofibroblasts expressing αSMA in response to the pro-fibrotic cytokine transforming growth factor-beta 1 (TGF-β1).

Chronic wound fibroblasts (CWFs) can be used as a model for understanding the signalling pathways involved in TGF-β1 driven fibroblast differentiation.

Chronic wounds are skin wounds that fail to heal. In chronic wounds, the fibroblast cells that normally differentiate into contractile myofibroblasts to close the wounds don’t respond to the pro-fibrotic cytokine transforming growth factor-beta 1 (TGF-β1) and fail to differentiate.

Research aim

1.Characterize CWFs response to TGF-β1

2. Determine the role of Hyaluronic acid synthase 1 (HAS1) expression in defective CWFs differentiation

3. Examine the defective protein transport and localisation in CWF

Mr Glyn Morris

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