Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Arteriosclerosis, Thrombosis, and Vascular Biology. 1990;10:198-207

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levin, R. I.
Right arrow Articles by Jaffe, E. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levin, R. I.
Right arrow Articles by Jaffe, E. A.

Arteriosclerosis, Vol 10, 198-207, Copyright © 1990 by American Heart Association

ARTICLES

Uremic levels of oxalic acid suppress replication and migration of human endothelial cells

RI Levin, PW Kantoff and EA Jaffe
Division of Cardiology, New York University School of Medicine, New York.

Patients with chronic renal failure who undergo hemodialysis experience accelerated atherosclerosis and premature death. Since the end- metabolite, oxalic acid, accumulates in plasma in proportion to the severity of renal failure, we studied whether sodium oxalate (0 to 300 microM) is an endothelial toxin and, therefore, might enhance atherogenesis. Exposure to uremic levels of oxalate (greater than 30 microM) for 9 to 28 days depressed endothelial cell replication by 33% to 84% (mean +/- SD, 54% +/- 15.7%, n = 17 experiments, p = 0.002). In contrast, replication of fibroblasts exposed to 200 microM oxalate for 45 days was not inhibited. The inhibitory effect of oxalate on endothelial cell replication was both dose- and time-dependent (both p less than 0.0001) and was first detected 3 to 7 days after the initial exposure to oxalate. Further, the inhibitory effect was fully reversible upon removal of oxalate, but only if exposure was limited to 5 days or less. Sodium salts of other carboxylic acids (citric, succinic, glyoxylic, and malonic; 200 microM) as well as HCl (200 microM) did not suppress endothelial cell replication. Oxalate also inhibited endothelial cell migration but had no effect on basal, thrombin-induced, or arachidonate-induced prostacyclin production by endothelial cells. Exposure of endothelial cells to sodium oxalate (200 microM) for as little as 24 hours-a time period sufficient to induce delayed, transient inhibition of replication not detectable until approximately 1 week after exposure-inhibited incorporation of 3H- leucine into protein by 40% (p = 0.009). We conclude that sodium oxalate acts as a uremic toxin, inhibiting endothelial cell replication and migration, functions which may be important for constitutive inhibition of atherosclerosis.


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
H. Cardinal, M.-A. Raymond, M.-J. Hebert, and F. Madore
Uraemic plasma decreases the expression of ABCA1, ABCG1 and cell-cycle genes in human coronary arterial endothelial cells
Nephrol. Dial. Transplant., February 1, 2007; 22(2): 409 - 416.
[Abstract] [Full Text] [PDF]


ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 1990 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.