An ultrastructural study of the contact between type I collagen assemblies and the induced human platelet aggregates.
Several type I collagen assemblies have been tested for their ability to induce platelet aggregation: a molecular solution, native and reconstituted native-type fibrils, segment long spacing aggregates (SLS) and an unordered collagen multimer. The ultrastructure of the inducer has been observed before its introduction into the platelet suspension as well as within the final aggregates. The following results have been obtained: 1) platelet aggregation was induced by the monomeric solution of collagen only after a long lag phase. While the original solution did not contain fibrillar elements, the platelet aggregates were in contact with collagen filaments showing a faint banding pattern. The results confirm that the longer lag time recorded is necessary for the collagen to polymerize and that the monomeric collagen actually does not induce platelet aggregation; 2) native and reconstituted native-type fibrils, SLS and unordered collagen multimer similarly induce platelet aggregation and were not modified during the course of this phenomenon; 3) although the general ultrastructure of the contacts between platelet and collagen assemblies were similar, a difference was noted in the extent of contact: a focal zone with native-type fibrils, numerous zones of contact with SLS and very extensive contact with unordered multimer. These results suggest that the combination of three factors are necessary to trigger platelet activation by collagen: the nature of the active sites on collagen, the density of these sites and the geometry of the collagen assembly.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects* / Q000648:ultrastructure; D002417:Cattle; D055598:Chemical Phenomena; D002621:Chemistry; D003094:Collagen / Q000494:pharmacology*; D006801:Humans; D008854:Microscopy, Electron; D010974:Platelet Aggregation; D013535:Suspensions
D013535:Suspensions; D003094:Collagen