Yamauchi Ryoko, Tanaka Makoto, Kume Noriaki, Minami Manabu, Kawamoto Takahiro, Togi Kiyonori, Shimaoka Takeshi, Takahashi Shu, Yamaguchi Junko, Nishina Takeshi, Kitaichi Masanori, Komeda Masashi, Manabe Toshiaki, Yonehara Shin, Kita Toru
Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Arterioscler Thromb Vasc Biol. 2004 Feb;24(2):282-7. doi: 10.1161/01.ATV.0000114565.42679.c6. Epub 2003 Dec 29.
SR-PSOX/CXCL16 is a transmembrane chemokine and is implicated in activated CD8+ T cell trafficking. In the present study, we examined the expression pattern of SR-PSOX/CXCL16 in the heart and investigated a potential role of SR-PSOX/CXCL16 in inflammatory valvular heart disease.
Initial expression of SR-PSOX/CXCL16 in murine embryos was detected in endothelial cells lining endocardial cushions in the forming heart at E11.5. From mid-gestation to adult, expression of this gene in the heart was exclusively observed in valvular endothelial cells. Examination of SR-PSOX/CXCL16 expression in human cardiac valves demonstrated that SR-PSOX/CXCL16 was strongly expressed in valvular and neocapillary endothelial cells in patients with infective endocarditis. SR-PSOX/CXCL16 expression in neocapillary endothelial cells was also observed in patients with rheumatic and atherosclerotic valvular disease. Moreover, CD8+ T cells were distributed closely to endothelial cells expressing SR-PSOX/CXCL16. In vitro adhesion assays showed that SR-PSOX/CXCL16 induced adhesion of activated CD8+ T cells to vascular cell adhesion molecule-1 (VCAM-1) through very late antigen-4 (VLA-4) activation. Furthermore, SR-PSOX/CXCL16 stimulated interferon-gamma (IFN-gamma) production by CD8+ T cells.
SR-PSOX/CXCL16 may be involved in CD8+ T cell recruitment through VLA-4 activation and stimulation of IFN-gamma production by CD8+ T cells during inflammatory valvular heart disease.
SR-PSOX/CXCL16是一种跨膜趋化因子，与活化的CD8+ T细胞迁移有关。在本研究中，我们检测了SR-PSOX/CXCL16在心脏中的表达模式，并研究了SR-PSOX/CXCL16在炎症性心脏瓣膜病中的潜在作用。
在胚胎期11.5天，在形成中心脏的心内膜垫内衬的内皮细胞中检测到小鼠胚胎中SR-PSOX/CXCL16的初始表达。从中孕期到成年期，该基因在心脏中的表达仅在内皮细胞中观察到。对人心脏瓣膜中SR-PSOX/CXCL16表达的检测表明，在感染性心内膜炎患者的瓣膜和新毛细血管内皮细胞中，SR-PSOX/CXCL16强烈表达。在风湿性和动脉粥样硬化性心脏瓣膜病患者中也观察到新毛细血管内皮细胞中SR-PSOX/CXCL16的表达。此外，CD8+ T细胞与表达SR-PSOX/CXCL16的内皮细胞紧密分布。体外黏附试验表明，SR-PSOX/CXCL16通过极晚期抗原-4（VLA-4）激活诱导活化的CD8+ T细胞与血管细胞黏附分子-1（VCAM-1）黏附。此外，SR-PSOX/CXCL16刺激CD8+ T细胞产生干扰素-γ（IFN-γ）。
在炎症性心脏瓣膜病期间，SR-PSOX/CXCL16可能通过VLA-4激活参与CD8+ T细胞募集，并刺激CD8+ T细胞产生IFN-γ。
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