Michael Bonner

TL;DR: It is demonstrated that systemic administration of CSD peptide to bleomycin-treated mice blocks epithelial cell apoptosis, inflammatory cell infiltration, and changes in tissue morphology as well as signaling molecule activation and collagen, tenascin-C, and ASMA expression associated with lung fibrosis.

TL;DR: The combined results demonstrate that a branched signaling pathway involving MEK, ERK, PKCϵ,PKCα, and caveolin-1 regulates collagen expression in normal lung tissue and is perturbed during fibrosis.

TL;DR: It is suggested that low caveolin-1 in S Sc monocytes contributes to ILD via effects on cell migration and phenotype and that the hyperaccumulation of fibrocytes in SSc-ILD may result from the altered phenotype and migratory activity of their monocyte precursors.

TL;DR: The data suggest that the PKC-gamma isoform increase observed afterThrombin stimulation is required for thrombin-induced IL-8 formation by human lung fibroblasts, consistent with the idea that upregulation ofIL-8 by throm bin in human lung Fibroblast requires cleavage of proteolytically activated receptor-I.

TL;DR: Caveolin-1 downregulation in leucocytes contributes to fibrotic lung disease, highlighting caveolin- 1 as a promising therapeutic target in scleroderma.