Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
Biochem Biophys Res Commun. 2012 Feb 24;418(4):662-8. doi: 10.1016/j.bbrc.2012.01.072. Epub 2012 Jan 24.
Thromboxane synthase (TXAS) is an enzyme that catalyzes the synthesis of thromboxane A(2) (TXA(2)). Overexpression of TXAS is associated with a variety of vascular diseases. Recently, we reported that visfatin, a novel adipokine, exhibits angiogenic actions. In this study, we showed that visfatin increased mRNA and protein levels of TXAS and stimulated TXA(2) biosynthesis in vascular endothelial cells. In addition, visfatin induced the expression and secretion of interleukin-8 (IL-8), which is blocked by a TXAS inhibitor and by the transfection of siRNA specific for TXAS. Furthermore, the inhibition of TXAS activity and blockade of the IL-8 receptor attenuated visfatin-induced endothelial angiogenesis. Together, these results showed that visfatin promoted IL-8 production by upregulation of TXAS, leading to angiogenic activation in endothelial cells.
血栓烷合酶（TXAS）是一种催化血栓烷 A2（TXA2）合成的酶。TXAS 的过度表达与多种血管疾病有关。最近，我们报道了一种新型脂肪因子内脂素具有血管生成作用。在本研究中，我们发现内脂素可增加血管内皮细胞中 TXAS 的 mRNA 和蛋白水平，并刺激 TXA2 的生物合成。此外，内脂素诱导白细胞介素-8（IL-8）的表达和分泌，而这种作用可被 TXAS 抑制剂和 TXAS 特异性 siRNA 的转染所阻断。此外，TXAS 活性的抑制和 IL-8 受体的阻断可减弱内脂素诱导的内皮血管生成。综上所述，这些结果表明，内脂素通过上调 TXAS 促进了 IL-8 的产生，从而导致内皮细胞的血管生成激活。
