The Adhesiveness of Human Blood Platelets in Vitro

The aggregation of blood platelets

“…The aggregation of platelets by ADP was first observed by Hellem (1960) who found that platelets were adsorbed on glass from citrated plasma only if erythrocytes were present; he isolated a substance from erythrocytes which induced this adsorption and which was later identified as ADP (Gaarder et al 1961). It is difficult to think of any physiological significance of this effect of ADP in red cells, except perhaps in the spleen.…”

Historical perspective on ADP-induced platelet activation

“…Several groups used selective P2Y 1 antagonists and showed that they inhibited ADP-induced shape change, aggregation, and increases in calcium, but not the effect of ADP on adenylyl cyclase [84,[114][115][116][117]. The P2Y 1 receptor is coupled to G q and activates phospholipase Cβ (PLCβ) [118] that is responsible for the formation of inositol (1,4,5)-trisphosphate (IP 3 ) and diacylglycerol, an activator of protein kinase C. IP 3 causes calcium mobilization from internal stores [118].…”

“…We have come a long way since 1960 when Hellem observed that a small molecule lost from red cells caused platelets to adhere to glass [1]. During the next year, Øllgaard [2] showed that this small molecule caused platelet aggregation, and it was identified as adenosine diphosphate (ADP) in Owren's laboratory [3].…”

PGE2 in the regulation of programmed erythrocyte death

“…25 Several lines of evidence indeed point to a role of erythrocytes in the regulation of hemostasis. [57][58][59][60] Beyond that, PGE 2 is a highly active mediator in inflammation, chemotactic processes, and cell damage (for review see Laufer 61 ). PGE 2 -dependent regulation of cation channels may also play a role in nucleated cells which similarly express cell volume regulatory cation channels.…”