Interleukin-16 polymorphism is associated with an increased risk of ischemic stroke.

Clinical and experimental data have demonstrated that inflammation plays fundamental roles in the pathogenesis of ischemic stroke. Interleukin-16 (IL-16) is identified as a proinflammatory cytokine that is a key element in the ischemic cascade after cerebral ischemia. We aimed to examine the relationship between the IL-16 polymorphisms and the risk of ischemic stroke in a Chinese population. A total of 198 patients with ischemic stroke and 236 controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing method. We found that the rs11556218TG genotype and G allele of IL-16 were associated with significantly increased risks of ischemic stroke (TG versus TT, adjusted OR = 1.88; 95% CI, 1.15-3.07; G versus T, adjusted OR = 1.54; 95% CI, 1.05-2.27, resp.). However, there were no significant differences in the genotype and allele frequencies of IL-16 rs4778889 T/C and rs4072111 C/T polymorphisms between the two groups, even after stratification analyses by age, gender, and the presence or absence of hypertension, diabetes mellitus, hypercholesterolemia, and hypertriglyceridemia. These findings indicate that the IL-16 polymorphism may be related to the etiology of ischemic stroke in the Chinese population.

Regulatory effects of the long non­coding RNA RP11­543N12.1 and microRNA­324­3p axis on the neuronal apoptosis induced by the inflammatory reactions of microglia.

The present study aimed to examine how the long non­coding RNA (lncRNA) RP11­543N12.1 interacted with microRNA (miR)­324­3p to modify microglials (MIs)­induced neuroblastoma cell apoptosis, which may pose benefits to the treatment of Alzhemier's disease (AD). The cell model of AD was established by treating SH­SY5Y cells with amyloid ß (Aß)25­35, and MI were acquired using primary cell culture technology. The lncRNAs that were differentially expressed between SH­SY5Y and control cells were screened through a microarray assay and confirmed via polymerase chain reaction. In addition, overexpression of RP11­543N12.1 and miR­324­3p was established by transfection of SH­SY5Y cells with pcDNA3.1(+)­RP11­543N12.1 and miR­324­3p mimics, respectively, while downregulation of RP11­543N12.1 and miR­324­3p was achieved by transfection with RP11­543N12.1­small interfering RNA (siRNA) and miR­324­3p inhibitor, respectively. The interaction between RP11­543N12.1 and miR­324­3p was confirmed with a dual­luciferase reporter gene assay. The results revealed that the expression levels of total and phosphorylated tau in SH­SY5Y cells were significantly elevated following Aß25­35 treatment (P<0.05), and RP11­543N12.1 was found to be differentially expressed between the control and Aß25­35­treated cells (P<0.05). Furthermore, the targeted association of RP11­543N12.1 and miR­324­3p was predicted based on miRDB4.0 and PITA databases, and then validated via the dual­luciferase reporter gene assay. SH­SY5Y cells transfected with siRNA or inhibitor, and treated with Aß25­35 displayed cellular survival and apoptosis that were similar to the normal levels (P<0.05). Finally, co­culture of MI and SH­SY5Y cells transfected with RP11­543N12.1­siRNA/miR­324­3p inhibitor significantly enhanced cell apoptosis (P<0.05). In conclusion, RP11­543N12.1 targeted miR­324­3p to suppress proliferation and promote apoptosis in the AD cell model, suggesting that RP11­543N12.1 and miR­324­3p may be potential biomarkers and therapeutic targets for AD.