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Recent studies have indicated that the deficiency of A Disintegrin-like and Metalloprotease with Thrombospondin Type 1 Motif, 13 (ADAMTS13) is a cause of TTP.
Thrombospondin 1, a mediator of the antiangiogenic effects of low-dose metronomic chemotherapy.
They describe comparison of the regulation of lymphatic and blood vessel development; key molecular regulators of angiogenesis; antiangiogenic agents such as thrombospondins and semaphorins; the role of the tumor microenvironment; blood vessel normalization for facilitating drug delivery; vascular pathologies such as hemangiomas, preeclampsia, and arteriovenous malformation, as well as the role of polymorphisms, integrins, and disruption of EC-EC junctions; and a critique of anti-vascular endothelial growth factor (VEGF) therapy, based on clinical trial information.
Several receptors including CD36 (6), thrombospondin (7), intercellular adhesion molecule-1 (8), vascular cell adhesion molecule, and E-selectin (9) mediate this interaction.
Gene encoding the collagen type I and thrombospondin receptor CD36 is located on chromosome 7q11.
Independent studies in 1996 by Furlan (10) and Tsai (12) identified V WF-cp as 1 of 19 members of the ADAMTS (A Disintegrinlike And Metalloprotease domain with ThromboSpondin type motifs) family of metalloproteases, designated ADAMTS-13.
A novel brain-specific p53-target gene, BAI1, containing thrombospondin type 1 repeats inhibits experimental angiogenesis.
Flow cytometric studies in whole blood show increased platelet surface expression of P-selectin, increased binding of thrombospondin to platelets and increased amounts of platelet-leukocyte aggregates in MPN patients compared to controls (22), (23).