Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2005;36:1189-1194
Published online before print May 5, 2005, doi: 10.1161/01.STR.0000166054.55993.e5
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
36/6/1189    most recent
01.STR.0000166054.55993.e5v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Blanco, M.
Right arrow Articles by Castillo, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Blanco, M.
Right arrow Articles by Castillo, J.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Stroke
Related Collections
Right arrow Cerebrovascular disease/stroke
Right arrow Mechanism of atherosclerosis/growth factors
Right arrow Risk Factors
Right arrow Ischemic biology - basic studies

(Stroke. 2005;36:1189.)
© 2005 American Heart Association, Inc.


Original Contributions

Increased Plasma Levels of 15-Deoxy {Delta} Prostaglandin J2 Are Associated With Good Outcome in Acute Atherothrombotic Ischemic Stroke

Miguel Blanco, MD, PhD; María Ángeles Moro, PhD; Antonio Dávalos, MD, PhD; Rogelio Leira, MD, PhD; Mar Castellanos, MD, PhD; Joaquín Serena, MD, PhD; José Vivancos, MD, PhD; Manuel Rodríguez-Yáñez, MD; Ignacio Lizasoain, MD, PhD José Castillo, MD, PhD

From the Department of Neurology (M.B., R.L., M.R.-Y., J.C.), Hospital Clínico Universitario, University of Santiago de Compostela, Santiago de Compostela; the Department of Pharmacology (M.A.M., I.L.), School of Medicine, University Complutense de Madrid, Madrid; the Department of Neurosciences (A.D.), Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona; the Department of Neurology (M.C., J.S.), Hospital Universitario Doctor Josep Trueta, Girona; and the Department of Neurology (J.V.), Hospital Universitario La Princesa, Madrid, Spain.

Correspondence to José Castillo, Servicio de Neurología- Sección Neurovascular y Unidad de Ictus, Hospital Clínico Universitario, Travesa da Choupana, s/n, 15706 Santiago de Compostela, Spain. E-mail mecasti{at}usc.es

Background and Purpose— The 15-deoxy {Delta} prostaglandin J2 (15-dPGJ2) is an anti-inflammatory prostaglandin that has been proposed to be the endogenous ligand of peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}), a nuclear receptor that can exert potent anti-inflammatory actions by repressing inflammatory genes when activated. It has been suggested that 15-dPGJ2 could be beneficial in neurological disorders in which inflammation contributes to cell death such as stroke.

Methods— We investigated the relationship between plasma levels of 15-dPGJ2 and early neurological deterioration (END), infarct volume, and neurologic outcome in 552 patients with an acute stroke admitted within 24 hours after symptoms onset.

Results— Median [quartiles] plasma 15-dPGJ2 levels on admission were significantly higher in patients than in controls (60.5 [11.2 to 109.4] versus 5.0 [3.8 to 7.2] pg/mL; P<0.0001). Levels of this prostaglandin were also significantly higher in patients with vascular risk factors (history of hypertension or diabetes) and with atherothrombotic infarcts (113.9 [81.6 to 139.7] pg/mL), than in those with lacunar (58.7 [32.7 to 86.2] pg/mL), cardioembolic (12.1 [6.5 to 39.2] pg/mL), or undetermined origin infarcts (11.4 [5.6 to 24.3] pg/mL) (P<0.0001). In the subgroup of patients with atherothrombotic infarcts, the adjusted odds ratio of END and poor outcome for 1 pg/mL increase in 15-dPGJ2 were 0.95 (95% CI, 0.94 to 0.97) and 0.97 (95% CI, 0.96 to 0.98), respectively. In a generalized linear model, by 1 U increase in 15-dPGJ2, there was a reduction of 0.47 mL (95% CI, 0.32 to 0.63) in the mean estimated infarct volume.

Conclusions— Increased plasma 15-dPGJ2 concentration is associated with good early and late neurological outcome and smaller infarct volume. These findings suggest a neuroprotective effect of 15-dPGJ2 in atherothrombotic ischemic stroke.


Key Words: atherosclerosis • diabetes mellitus • hypertension • inflammation • stroke




This article has been cited by other articles:


Home page
Therapeutic Advances in Cardiovascular DiseaseHome page
M. Collino, N. S.A. Patel, and C. Thiemermann
Review: PPARs as new therapeutic targets for the treatment of cerebral ischemia/reperfusion injury
Therapeutic Advances in Cardiovascular Disease, June 1, 2008; 2(3): 179 - 197.
[Abstract] [PDF]


Home page
Mol. Pharmacol.Home page
T. E. Taylor-Clark, B. J. Undem, D. W. MacGlashan Jr., S. Ghatta, M. J. Carr, and M. A. McAlexander
Prostaglandin-Induced Activation of Nociceptive Neurons via Direct Interaction with Transient Receptor Potential A1 (TRPA1)
Mol. Pharmacol., February 1, 2008; 73(2): 274 - 281.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
J. F. Arenillas, M. A. Moro, and A. Davalos
The Metabolic Syndrome and Stroke: Potential Treatment Approaches
Stroke, July 1, 2007; 38(7): 2196 - 2203.
[Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
K. T. Chambers, S. M. Weber, and J. A. Corbett
PGJ2-stimulated beta-cell apoptosis is associated with prolonged UPR activation
Am J Physiol Endocrinol Metab, April 1, 2007; 292(4): E1052 - E1061.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
S.-W. Park, J.-H. Yi, G. Miranpuri, I. Satriotomo, K. Bowen, D. K. Resnick, and R. Vemuganti
Thiazolidinedione Class of Peroxisome Proliferator-Activated Receptor {gamma} Agonists Prevents Neuronal Damage, Motor Dysfunction, Myelin Loss, Neuropathic Pain, and Inflammation after Spinal Cord Injury in Adult Rats
J. Pharmacol. Exp. Ther., March 1, 2007; 320(3): 1002 - 1012.
[Abstract] [Full Text] [PDF]