PubMed · 997001
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A Beaulieu, H A Menard. 1976. [Scleroderma: what is it].. https://pubmed.ncbi.nlm.nih.gov/997001/
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Conditioned media from cultures of human metastatic Hs294T melanoma cells contain a factor/factors that promote(s) fibroblast-mediated contraction of collagen lattices, and stimulate(s) fibroblast glycosaminoglycan (GAG) synthesis. Complete medium from melanoma cell cultures stimulated fibroblast hyaluronate synthesis 9.3-fold, and sulphated GAG synthesis 2.6-fold, as measured by 3H-glucosamine incorporation. 35SO4 incorporation into sulphated GAGS was essentially unaltered, the net result being a decrease in the degree of sulphation. Fibroblasts synthesized hyaluronate with an increased molecular weight when grown in the presence of the melanoma-cell culture medium, while the molecular weights of heparan and chondroitin sulphates remained essentially unaltered. Our results indicate that the tumour-cell-derived factor(s) stimulate(s) changes in fibroblast glycosaminoglycan synthesis, and that these changes may facilitate tumour cell invasion in vivo.
The hydroxamic acid HONHCOCH2CH(i-Bu)CO-L-Trp-NHMe, isomer 6A (GM 6001), inhibits human skin fibroblast collagenase with Ki of 0.4 nM using the synthetic thiol ester substrate Ac-Pro-Leu-Gly-SCH(i-Bu)CO-Leu-Gly-OEt at pH 6.5. The other isomer, 6B, which has the opposite configuration at the CH2CH(i-Bu)CO alpha-carbon atom, has a Ki of 200 nM for this enzyme. GM 6001 is one of the most potent inhibitors of human skin fibroblast collagenase yet reported. GM 6001 has a Ki of 20 nM against thermolysin and Pseudomonas aeruginosa elastase. Isomer 6B has a Ki of 7 nM against thermolysin and 2 nM against the elastase. 6A and 6B are the most potent hydroxamate inhibitors reported for these bacterial enzymes. The pattern of inhibition for all three enzymes suggests that isomer 6A is the (R,S) compound, stereochemically analogous to the L,L-dipeptide, and isomer 6B is the (S,S) compound, analogous to the DL-dipeptide. The tolerance of the D configuration by thermolysin and the elastase allows these inhibitors to discriminate between the human and bacterial enzymes simply by inversion of configuration at the CH2CH(i-Bu)CO alpha-carbon atom. Substitution of the potential metal liganding groups carboxylate and hydrazide for the hydroxamate group yields much weaker inhibitors for all three enzymes.
In an effort to elucidate the mechanism of liver damage resulting from Hepatitis A virus (HAV) infection, we have studied infected skin fibroblasts and autologous lymphocytes from HAV patients. We report here that HLA-restricted virus-specific T cells play an essential role in HAV-related hepatocellular injury.