Ruan Ke-He, So Shui-Ping, Wu Hanjing, Cervantes Vanessa
Department of Pharmacological and Pharmaceutical Sciences, Center for Experimental Therapeutics and PharmacoInformatics, College of Pharmacy, University of Houston, Science & Research Building 2, Room 521, Houston, TX 77204-5037, USA.
Arch Biochem Biophys. 2008 Dec 1;480(1):41-50. doi: 10.1016/j.abb.2008.09.010. Epub 2008 Sep 22.
Recently, we reported that a novel hybrid enzyme (TriCat enzyme), engineered by linking human cyclooxygenase-2 (COX-2) with prostacyclin (PGI(2)) synthase (PGIS) together through a transmembrane domain, was able to directly integrate the triple catalytic (TripCat) functions of COX-2 and PGIS and effectively convert arachidonic acid (AA) into the vascular protector, PGI(2) [K.H. Ruan, H. Deng, S.P. So, Biochemistry 45 (2006) 14003-14011]. In order to confirm the important biological activity and evaluate its therapeutic potential, it is critical to characterize the properties of the enzyme using the purified protein. The TriCat enzyme cDNA was subcloned into a baculovirus vector and its protein was expressed in Sf-9 cells in large-scale with a high-yield ( approximately 4% of the total membrane protein), as confirmed by Western blot and protein staining. The Sf-9 cells' membrane fraction, rich in TriCat enzyme, exhibited strong TriCat functions (K(m)=3 microM and K(cat)=100 molecules/min) for the TriCat enzyme and was 3-folds faster in converting AA to PGI(2) than the combination of the individual COX-2 and PGIS. Another superiority of the TriCat enzyme is its dual effect on platelet aggregation: it completely inhibited platelet aggregation at the low concentration of 2 microg/ml and then displayed the ability to reverse the initially aggregated platelets to their non-aggregated state. Furthermore, multiple substrate-binding sites were confirmed in the single protein by high-resolution NMR spectroscopy, using partially purified TriCat enzyme. These studies have clearly demonstrated that the isolated TriCat enzyme protein functions in the selective biosynthesis of the vascular protector, PGI(2), and revealed its potential for anti-thrombosis therapeutics.
最近,我们报道了一种新型杂交酶(TriCat酶),它是通过跨膜结构域将人环氧化酶-2(COX-2)与前列环素(PGI₂)合酶(PGIS)连接在一起构建而成的,能够直接整合COX-2和PGIS的三重催化(TriCat)功能,并有效地将花生四烯酸(AA)转化为血管保护剂PGI₂ [阮克华,邓华,苏树鹏,《生物化学》45 (2006) 14003 - 14011]。为了证实其重要的生物活性并评估其治疗潜力,使用纯化的蛋白质来表征该酶的特性至关重要。将TriCat酶的cDNA亚克隆到杆状病毒载体中,并在Sf-9细胞中大量高产表达(约占总膜蛋白的4%),这通过蛋白质免疫印迹和蛋白质染色得以证实。富含TriCat酶的Sf-9细胞膜组分对TriCat酶表现出很强的TriCat功能(米氏常数Kₘ = 3微摩尔,催化常数Kcat = 100分子/分钟),并且在将AA转化为PGI₂方面比单独的COX-2和PGIS组合快3倍。TriCat酶的另一个优势在于其对血小板聚集的双重作用:在低浓度2微克/毫升时它能完全抑制血小板聚集,然后还表现出将最初聚集的血小板逆转至非聚集状态的能力。此外,利用部分纯化的TriCat酶,通过高分辨率核磁共振光谱在单一蛋白质中证实了多个底物结合位点。这些研究清楚地表明,分离得到的TriCat酶蛋白在血管保护剂PGI₂的选择性生物合成中发挥作用,并揭示了其在抗血栓治疗方面的潜力。