No Association of PLIN Polymorphisms With Hemorrhagic and Ischemic Stroke

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. 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. 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). 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.