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Figure 2 | Fibrogenesis & Tissue Repair

Figure 2

From: Thrombospondin 1 is a key mediator of transforming growth factor β-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism

Figure 2

Blocking thrombospondin 1 (TSP1) signalling with a LSKL peptide reduces matrix protein expression in both systemic sclerosis (SSc) and normal fibroblasts. (a) Following contraction in the culture force monitor (CFM) the LSKL peptide-treated fibroblasts were prepared for western blot analyse to determine the protein expression levels. LSKL peptide reduced the expression of some profibrotic proteins and mitogen-activated protein kinase (MAPK) activities in SSc fibroblasts. (b) Immunofluorescence staining demonstrated that the LSKL peptide-treated SSc fibroblasts demonstrated a reduction in α smooth muscle actin (α-SMA) stress fibres and reduced the presence of p-extracellular signal-regulated kinase (ERK).

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