By Carolyn A. Staton, Claire Lewis, Roy Bicknell
Content material:
Chapter 1 Endothelial mobilephone Biology (pages 1–38): Femke Hillen, Veerle Melotte, Judy R. van Beijnum and Arjan W. Griffioen
Chapter 2 Endothelial telephone Proliferation Assays (pages 39–50): Wen?Sen Lee
Chapter three Endothelial mobilephone Migration Assays (pages 51–64): Christos Polytarchou, Maria Hatziapostolou and Evangelia Papadimitriou
Chapter four Tubule Formation Assays (pages 65–87): Ewen J. Smith and Carolyn A. Staton
Chapter five Modelling the consequences of the Haemodynamic setting on Endothelial mobile Responses suitable to Angiogenesis (pages 89–103): Gerard B. Nash and Stuart Egginton
Chapter 6 complete or Partial Vessel Outgrowth Assays (pages 105–121): Cindy H. Chau and William D. Figg
Chapter 7 Assaying Endothelial–Mural phone Interactions (pages 123–137): Melissa ok. Nix and Karen ok. Hirschi
Chapter eight Assays for Membrane and Intracellular Signalling occasions (pages 139–166): Vittorio Tomasi, Cristiana Griffoni, Spartaco Santi, Patrizia Lenaz, Rosa Anna Iorio, Antonio Strillacci and Enzo Spisni
Chapter nine Implantation of Sponges and Polymers (pages 167–182): Silvia P. Andrade, Monica A. N. D. Ferreira and Tai?Ping Fan
Chapter 10 Angiogenesis Assays within the Chick (pages 183–201): Andries Zijlstra, David Mikolon and Dwayne G. Stupack
Chapter eleven Corneal Angiogenesis Assay (pages 203–228): Siqing Shan and Mark W. Dewhirst
Chapter 12 Dorsal Air Sac version (pages 229–238): Sei Yonezawa, Tomohiro Asai and Naoto Oku
Chapter thirteen Chamber Assays (pages 239–263): Michael D. Menger, Matthias W. Laschke and Brigitte Vollmar
Chapter 14 Tumour versions: research of Angiogenesis in vivo (pages 265–291): Sven A. Lang and Oliver Stoeltzing
Chapter 15 Angiomouse: Imageable types of Angiogenesis (pages 293–310): Robert M. Hoffman
Chapter sixteen options and Advances in Vascular Imaging in Danio Rerio (pages 311–326): Kenna R. generators Shaw and Brant. M. Weinstein
Chapter 17 organic and medical Implications of Recruitment of Stem Cells into Angiogenesis (pages 327–340): Gianluigi Castoldi, Antonio Cuneo and Gian Matteo Rigolin
Chapter 18 equipment for tracking of the Anti?Angiogenic task of brokers in sufferers: Novel Trial layout (pages 341–359): Shannon Smiley, Michael ok. okay. Wong and Shaker A. Mousa
Chapter 19 an outline of present Angiogenesis Assays: selection of Assay, Precautions in Interpretation, destiny necessities and instructions (pages 361–374): Robert Auerbach
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Angiogenesis Assays: A Critical Appraisal of Current Techniques
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Additional resources for Angiogenesis Assays: A Critical Appraisal of Current Techniques
Sample text
Endothelial cells have also other cell-specific homophilic adhesion proteins at the intercellular contacts. Two of the most studied are platelet endothelial cell adhesion molecule-1 (PECAM-1) and S-endo-1, both members of the immunoglobulin superfamily. The amino-terminal immunoglobulin-like domain of PECAM-1 is involved in homophilic binding on adjacent cells. Other domains of this molecule are involved in heterophilic adhesive interactions with several ligands such as avb3, CD38 and several proteoglycans (Jackson, 2003).
In adults, it is involved in maturation and stabilization of mature vessels. Ang-2 is involved in postnatal angiogenic and vascular remodelling events and in detaching smooth muscle cells and loosening underlying matrix, thereby allowing endothelial cells to migrate as inter-endothelial cell contacts are relaxed (Thurston, 2003). Ang-2, in concert with VEGF, is also angiogenic, although in the absence of VEGF, Ang-2 may actually induce vessel regression. Transforming growth factor (TGF) is a multifunctional cytokine involved in proliferation, differentiation, migration and survival of many cell types (Sun, 2004).
Fibrinolytic activity of endothelial cells A fibrin matrix is formed after wounding of a blood vessel and after leakage of plasma from blood vessels in areas of inflammation and tumourigenesis. The fibrin matrix acts as a barrier preventing further blood leakage and it provides a structure for new microvessels to infiltrate in damaged or activated tissue (Dvorak, 2000). Whenever a blood clot is formed, a large amount of plasminogen is trapped in the clot along with other plasma proteins (Guyton, 2005).