WFRF:(Dixelius Johan)
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- Dixelius, Johan,1958-Uppsala universitet,Institutionen för genetik och patologi (author)
Endothelial differentiation and angiogenesis regulation
- BookEnglish2002
Publisher, publication year, extent ...
- Uppsala :Acta Universitatis Upsaliensis,2002
- 47 s.
- electronicrdacarrier
Numbers
- LIBRIS-ID:oai:DiVA.org:uu-3009
- ISBN:9155454607
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3009URI
Supplementary language notes
- Language:English
- Summary in:English
Part of subdatabase
- SwePubSwePub
Classification
Series
- Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,0282-7476 ;1205
Notes
- Angiogenesis can be defined as the formation of new blood vessels from pre-existing ones. Angiogenesis is required for development and maintenance of our vascular system and thus of fundamental importance to our existence. The endothelial cells that line the inside of the vessels de-differentiate, migrate, proliferate and re-differentiate during angiogenesis. Angiogenesis is tightly regulated, controlled by several angiogenic factors of various classes that promote angiogenesis but also by anti-angiogenic factors that counteract the effect of the pro-angiogenic factors. We have examined three factors involved in angiogenesis regulation, Vascular endotelial growth factor (VEGFR) -3, the matrix protein laminin-1 and the collagen XVIII derived fragment endostatin. Five tyrosine phosphorylation sites in the cytoplasmic tail of VEGFR-3 were identified by phosphopeptide mapping (PPM). The data was confirmed by PPM using point-mutated receptors generated by site-directed mutagenesis.Laminin-1 was found to promote angiogenesis in the chicken chorioallantoic membrane assay and in a synergistic fashion together with suboptimal levels of fibroblast growth factor 2 (FGF-2) in embryoid bodies. Laminin-1 also promoted endothelial tubular morphogenesis in vitro, and upregulated the expression of the endothelial differentiation marker Jagged-1. Endostatin was shown to affect endothelial FGF-2-induced cell survival and morphogenesis. This was a result of direct binding to endothelial cells and induction of tyrosine phosphorylation of many proteins including the adaptor protein Shb. The apoptotic and morphogenic responses induced by endostatin was shown to be dependent on Shb. Further, endostatin inhibited endothelial migration and affected molecules implicated in migration. In particular, FGF-2 induced actin reorganization, and β-catenin regulation was modulated by endostatin.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Medicinsk genetik hsv//swe
- MEDICAL AND HEALTH SCIENCES Basic Medicine Medical Genetics hsv//eng
- Genetics
- Angiogenesis
- VEGFR-3
- Laminin
- endostatin
- FGF-2
- b-catenin
- Genetik
- Clinical genetics
- Klinisk genetik
- Molecular Medicine
- molekylär medicin (genetik och patologi)
Added entries (persons, corporate bodies, meetings, titles ...)
- Olsen, Björn (opponent)
- Uppsala universitetInstitutionen för genetik och patologi (creator_code:org_t)
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