A synthetic peptide derived from the sequence of a type I collagen receptor inhibits type I collagen-mediated platelet aggregation

Thomas M. Chiang, Andrew Kang

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

A synthetic peptide-1, an 18 amino acid residue peptide derived from a hydrophilic domain of a cloned platelet type I collagen receptor, was used to study the role of the receptor on types I and III collagen-induced platelet aggregation and the release of ATP. The peptide inhibits the type I, but not the type III, collagen-induced platelet aggregation and the release of ATP in a dose-dependent manner. The [125I]peptide-1 specifically binds to type I collagen-coated microtiter wells in a dose-dependent manner (with K(d) = 10 nM). The binding of [125I]peptide-1 can be inhibited by an excess of unlabeled peptide-1 suggesting that the binding is specific. The labeled peptide-1 does not bind to type III collagen-coated microtiter wells. Results from an enzyme-linked immunosorbent assay show that the peptide reacts with the poly- and monoclonal antibodies raised against the purified platelet type I collagen receptor (M(r) 65 kD). The peptide also inhibits the adhesion of platelets on type I collagen matrix and rabbit aortic segments in a dose- dependent manner. These results suggest that the reactive site of the platelet receptor for type I collagen resides in this portion of the molecule.

Original languageEnglish (US)
Pages (from-to)2079-2084
Number of pages6
JournalJournal of Clinical Investigation
Volume100
Issue number8
DOIs
StatePublished - Oct 15 1997

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Collagen Type I
Platelet Aggregation
Peptides
Blood Platelets
Collagen Type III
Adenosine Triphosphate
type I collagen receptor
Catalytic Domain
Enzyme-Linked Immunosorbent Assay
Monoclonal Antibodies
Rabbits
Amino Acids

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

A synthetic peptide derived from the sequence of a type I collagen receptor inhibits type I collagen-mediated platelet aggregation. / Chiang, Thomas M.; Kang, Andrew.

In: Journal of Clinical Investigation, Vol. 100, No. 8, 15.10.1997, p. 2079-2084.

Research output: Contribution to journalArticle

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