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Figure 1 | Fibrogenesis & Tissue Repair

Figure 1

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 1

The enhanced contractile activity of fibrotic systemic sclerosis (SSc) fibroblasts can be moderated by blocking thrombospondin 1 (TSP1) activation of latent transforming growth factor (TGF)β with a LSKL peptide. Normal and SSc fibroblasts were pretreated for 5 days with LSKL peptide, a selective antagonist of TSP1. Cells were then suspended in a collage lattice prior to contraction in the culture force monitor (CFM). Blocking the TSP1 function with the LSKL peptide reduced the force generated by both normal and SSc cells even after treatment with TGFβ. Note that LSKL peptide also reduced the basal contractile force in normal fibroblasts groups. SLLK peptide was used as an inert control.

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