科研之友
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摘要
ObjectiveSmoking is a recognized cardiovascular risk factor. Perivascular visceral adipose tissue (PVAT) is a source of inflammatory molecules, thus contributing to atherosclerosis progression. The P2X(7) receptor (P2X(7)R)-inflammasome complex, crucial in determining IL-1 and IL-18 release, participates in this scenario. We evaluated whether smoking might affect the PVAT inflammatory phenotype and explored the putative role of the axis P2X(7)R-inflammasome in this picture. Subjects and MethodsTNF, IL-6, RBP4, MCP-1, as well as P2X(7)R and inflammasome components NLRP3, ASC, caspase-1 and IL-1 and IL-18 expression was determined in adipocytes isolated by PVAT of healthy smokers (Smok) and nonsmokers (No-Smok) subjects. Plasma and culture medium levels of these cytokines were also determined. ResultsPerivascular adipose tissue of Smok had a higher expression of P2X(7)R and inflammasome components; via P2X(7)R activation, it released more IL-1 and IL-18, whose serum levels were also higher in Smok than in No-Smok. Linear correlations of NLRP3 with P2X(7)R and IL-18 expression and release emerged. Smok also had a higher PVAT expression of the chemotactic factor MCP-1. However, no difference was observed in the PVAT expression of genes more strictly related to insulin resistance, like TNF, RBP4, IL-6; this was coupled with similar plasma levels of TNF and RBP4 in the two groups. ConclusionSmoking contributes to the pro-inflammatory status of the PVAT by enhancing expression and activity of the P2X(7)R-inflammasome complex; the effect on adipocytokines more related to insulin resistance and metabolic abnormalities appears trivial.
- 出版日期2014-3
