http://purl.uniprot.org/citations/20195245 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/20195245 | http://www.w3.org/2000/01/rdf-schema#comment | "Wound healing and sclerosis are characterized by an increase of extracellular matrix proteins, which are characteristically expressed in the embryo-fetal period. We analyzed the expression of fibrillin-2, which is typically found in embryonic tissues, but only scarcely in adult skin. In wound healing and sclerotic skin diseases such as lipodermatosclerosis and scleroderma, a marked increase of fibrillin-2 expression was found by immunohistology. Double labelling of fibrillin-2 and tenascin-C, which is also expressed in wound healing and sclerosis, showed co-localization of both proteins. Solid-phase and slot blot-overlay assays showed a dose-dependent binding of the recombinant N-terminal half of fibrillin-2 (rFBN2-N) to tenascin-C. Real-time PCR showed an increase of the fibrillin-2 gene expression in cell culture triggered by typical mediators for fibroblast activation such as serum, IL-4, and TGF-beta. By contrast, prolonged hypoxia is not associated with changes in fibrillin-2 expression. Tenascin-C is an anti-adhesive substrate for fibroblasts, whereas fibrillin-2 stimulates cell attachment. Attachment assays using mixed substrates showed decreased cell attachment when tenascin-C and rFBN2-N were coated together, compared with the attachment to rFBN2-N alone. Fibrillins are involved in storage and activation of TGF-beta. Immunohistology with an antibody against the latency-associated peptide (LAP (TGF-beta1)) showed a marked increase of inactive LAP-bound TGF-beta1 in wound healing and sclerotic skin whereas normal skin showed only a weak expression. Double immunofluorescence confirmed a partial colocalization of both proteins. In conclusion, we show that a stimulation of the fibrillin-2 expression is a characteristic feature of fibroblasts present in wound healing and sclerosis, which may be involved in the alteration of cell attachment and storage of inactive TGF-beta in the matrix."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.org/dc/terms/identifier | "doi:10.1038/labinvest.2010.49"xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Kramer J."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Reinhardt D.P."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Gibson M.A."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Kahle B."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Brinckmann J."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Hubmacher D."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Rohwedel J."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/author | "Hunzelmann N."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/name | "Lab Invest"xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/pages | "739-752"xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/title | "Enhanced fibrillin-2 expression is a general feature of wound healing and sclerosis: potential alteration of cell attachment and storage of TGF-beta."xsd:string |
http://purl.uniprot.org/citations/20195245 | http://purl.uniprot.org/core/volume | "90"xsd:string |
http://purl.uniprot.org/citations/20195245 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20195245 |
http://purl.uniprot.org/citations/20195245 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/20195245 |
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