This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Robson, S. C. Articles by Drosopoulos, J. H.F. Search for Related Content PubMed PubMed Citation Articles by Robson, S. C. Articles by Drosopoulos, J. H.F.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1251.)
© 2001 American Heart Association, Inc.

Letters to the Editor

Thromboregulation by Endothelial Cells: Significance for Occlusive Vascular Diseases

Simon C. Robson

Associate Professor of Medicine Harvard Medical School Boston, Massachusetts

To the Editor:

I wish to raise several issues about the "Brief Review" by Dr Aaron J. Marcus and colleagues.

The prior ecto-ADPase or ATP diphosphohydrolase nomenclature is no longer recommended; nucleoside triphosphate diphosphohydrolase or NTPDase is the preferred terminology for this family of enzymes. For example, CD39 can now be classified as NTPDase-1.¹

The claim here (and in prior communications) that work by Dr Marcus and colleagues² was "the first direct demonstration of a physiological function for CD39 ... blockade of platelet responsiveness to ... ADP" is incorrect. Prior to this, we had clearly demonstrated that CD39 cloned from human umbilical vein endothelial cells had all the biochemical and biological properties (inclusive of platelet antiaggregatory capacity) of an ecto-ADPase or ATPDase (old terminology).³ In addition, the pioneering work of Miura and colleagues,⁴ who demonstrated that the major antiaggregatory activity of bovine aorta microsomes for ADP-induced aggregation was due to an ATPDase, has not been referred to. Beaudoin and colleagues⁵ had also shown that partially purified ATPDases from bovine aorta had important platelet-regulatory properties, but this work was unfortunately overlooked.

The statement that "collagen and TRAP depend more on released ADP for recruitment and aggregation than was previously appreciated" was based solely on data in Gayle et al.⁶ Prior to this manuscript, we had documented that CD39 inhibits platelet aggregation to ADP, collagen, and thrombin³ ; additionally, platelets from the mutant mouse null for cd39 are nonresponsive to collagen and thrombin.⁷

The important cysteine at the N-terminal end of . . . [Full Text of this Article]

Aaron J. Marcus; M. Johan Broekman; Joan H.F. Drosopoulos

Hematology-Oncology, VA–NewYork Harbor Healthcare System, Weill Medical College of Cornell University, New York, New York