Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2008;39:470-472
Published online before print January 3, 2008, doi: 10.1161/STROKEAHA.107.496026
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
39/2/470    most recent
STROKEAHA.107.496026v1
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 Google Scholar
Google Scholar
Right arrow Articles by Song, W.
Right arrow Articles by Hui, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Song, W.
Right arrow Articles by Hui, R.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
Medline Plus Health Information
*Stroke
Related Collections
Right arrow Genetics of Stroke

(Stroke. 2008;39:470.)
© 2008 American Heart Association, Inc.


Research Letters

No Association of PLIN Polymorphisms With Hemorrhagic and Ischemic Stroke

Weihua Song, MD; Jingzhou Chen, PhD; Kai Sun, PhD; Hui Yu, MS Rutai Hui, MD, PhD

From the Key Laboratory of Clinical Cardiovascular Genetics, Ministry of Education and Sino-German Laboratory for Molecular Medicine, Hypertension Division, FuWai Hospital, Chinese Academy of Medical Sciences, Beijing, P.R. China.

Correspondence to Rutai Hui, MD, PhD, FuWai Hospital, 167 Beilishilu, Beijing 100037, P.R. China. E-mail huirutai{at}sglab.org

Abstract

Background and Purpose— Perilipin is encoded by the gene PLIN and mediates lipid metabolism. Its upregulation has been linked to the formation of foam cells, rupture of atherosclerotic plaques, and perhaps acute coronary syndrome. We hypothesized that genetic variations in PLIN might contribute to the susceptibility to stroke. The hypothesis was tested in 2 case–control studies.

Methods— Six PLIN tag single nucleotide polymorphisms (rs7176403, rs8179078, rs6496589, rs8179043, rs894160, rs1052700) were genotyped in 1571 patients with stroke (690 cerebral thrombosis, 429 lacunar infarction, 452 intracerebral hemorrhage) and 1638 control subjects. A SHEsis software platform was used to analyze pairwise linkage disequilibrium and haplotype association in the case–control study. The study was replicated in another independent case–control study including 120 patients with stroke and 240 control subjects.

Results— No association of the PLIN variants with stroke (P>0.05) or with stroke subtypes (P>0.05) was found in the first study. The findings were confirmed in the second population (P>0.05).

Conclusions— The data represent an important negative finding that the common variants of PLIN do not have a major effect on susceptibility to stroke in a Chinese population.


Key Words: perilipin • polymorphism • risk factors • stroke