辛伐他汀对鼠平滑肌细胞脂质蓄积及CXCL16表达的影响
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摘要
目的观察oxLDL对鼠源平滑肌细胞脂质蓄积的影响。观察辛伐他汀对oxLDL诱导的鼠源平滑肌细胞脂质蓄积与影响。观察辛伐他汀对oxLDL诱导的泡沫细胞CXCL16表达的影响。
方法采用体外培养的SD大鼠平滑肌细胞作为研究对象,换含0.1%血清的培养基培养后加处理因素。
Ⅰ.不同浓度的oxLDL(0、20mg/L、40mg/L、60mg/L、80mg/L)与鼠源平滑肌细胞共同孵育24h和用60mg/L oxLDL与鼠源平滑肌细胞孵育不同时间即(0h、6h、12h、24h、36h),油红O染色观察细胞内脂质蓄积情况,高效液相色谱分析法检测细胞总胆固醇蓄积情况,Western blotting检测平滑肌细胞CXCL16蛋白质的表达。
Ⅱ.用60mg/L oxLDL与不同浓度的辛伐他汀(0uM、1uM、10uM、100uM)共同孵育24h,空白组作为对照组和用60mg/L oxLDL与最佳浓度的辛伐他汀100uM,同时孵育不同的时间即(0h、6h、12h、24h),空白组作为对照组,油红O染色观察细胞内脂质蓄积情况,高效液相色谱分析法检测细胞总胆固醇蓄积情况,Western blotting检测平滑肌细胞CXCL16蛋白质的表达。
结果Ⅰ.oxLDL诱导的鼠源平滑肌细胞脂质蓄积与oxLDL呈剂量依赖性和时间依赖性(P<0.05)。.油红O染色显示:与空白对照组和低浓度组比较,较高浓度的oxLDL组(60mg/L、80mg/L)诱导平滑肌细胞较oxLDL低浓度(20mg/L、40mg/L)组胞内脂滴明显增多,体积增大。oxLDL(60mg/L)较长时间(24h、36h)诱导平滑肌细胞比较短时间(0h、6h、12h)胞内脂滴明显增多,体积增大。在oxLDL浓度为0、20mg/L、40mg/L、60mg/L、80mg/L时,HPLC检测的CE/TC的比值分别为(10.78±1.25)%、(24.40±1.84)%、(35.6±2.47)%、(56.16±1.80)%(P<0.01) (57.50±2.47)%,在60mg/L的oxLDL作用的不同时间即(0h、6h、12h、24h、36h),HPLC检测的CE/TC的比值分别为(10.78±1.25)%、(23.78±1.80)%、(36.95±2.39)%、(55.39±2.22)%、(58.89±4.05)%(P<0.05)。
Ⅱ.辛伐他汀能抑制鼠源平滑肌细胞对oxLDL的摄取,油红O染色可见oxLDL+simvastatin组细胞内脂滴较oxLDL组明显减少,且脂滴颗粒体积变小。在oxLDL(60mg/L)与simvastatin浓度分别为(0uM、1uM、10uM、100uM)时,HPLC检测的CE/TC的比值分别为(57.28±0.83)%、( 55.06±2.05)%、(46.20±1.44)%、( 17.86±0.97)%.正常组的CE/TC的比值为(10.78±1.25)%(P<0.05).在oxLDL(60mg/L)与simvastatin(100uM)作用不同的时间组(0h、6h、12h、24h),HPLC检测的CE/TC的比值分别为(57.28±0.83)%、(34.74±1.21)%、(25.96±1.31)%、(17.86±0.97)%(P<0.01).
Ⅲ.在正常对照组和荷脂细胞(CE/TC<50%)组中,CXCL16蛋白表达无显著差异性(P>0.05),而在泡沫细胞(CE/TC>50%)组中,CXCL16蛋白表达显著增加,CXCL16的表达与细胞泡沫化有关(p<0.05)。辛伐他汀能降低泡沫细胞中的CXCL16的表达,且呈剂量依赖性和时间依赖性(P<0.05)。
结论1. oxLDL诱导鼠源平滑肌细胞脂质蓄积在一定范围内呈剂量依赖性和时间依赖性。
2.辛伐他汀明显降低泡沫细胞内的胆固醇酯与总胆固醇的比值,且在一定范围内呈剂量依赖性和时间依赖性。
3.辛伐他汀能降低泡沫细胞中的CXCL16的表达,且在一定的范围内呈剂量依赖性和时间依赖性。
Objective The purpose of the present study was to investigate the effect of oxLDL(oxidized low-density lipoprotein)-induced lipid accumulation in murine aortic smooth muscle cells, the effect of simvastatin on oxLDL-induced lipid accumulation in foam cells of murine aortic smooth muscle cells and the relation with CXCL16.
MethodsⅠ. Murine Aortic smooth muscle cells were incubated with oxLDL at different concentration (0、20、40、60、80mg/L) respectively for 24h,and murine Aortic smooth muscle cells were incubated with 60mg/L oxLDL at different time (0h、6h、12h、24h、36h).Oil red O staining was used to observe the intracellular lipid droplets.Cellular total cholesterol was determined by high performance liquid chromatography(HPLC) analysis. CXCL16 protein level was determined by Western blotting.
Ⅱ.Murine aortic smooth muscle cells were coincubated with 60mg/L oxLDL and simvastatin at different concentration (0uM、1uM、10uM、100uM) respectively for 24h, and murine aortic smooth muscle cells were coincubated with 60mg/L oxLDL and simvastatin of the best concentration respectively for 0h、6h、12h、24h. murine aortic smooth muscle cells were incubated without oxLDL and simvastatin as the control groups. Oil red O staining was used to observe the intracellular lipid droplets.Cellular total cholesterol was determined by high performance liquid chromatography(HPLC) analysis. CXCL16 protein level was determined by Western blotting.
ResultsⅠ. The oxLDL-induced lipid accumulation was in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner(P<0.05) .Oil red O staining showed the more lipid droplets were in higher concentration oxLDL(60mg/L,80mg/L) groups than lower concentration oxLDL (20mg/L、40mg/L) groups .and the more lipid droplets were in longer time (24h、36h) groups than shorter time(6h、12h) groups. HPLC analysis demonstrated the ratios of cellular CE/TC were 10.8%、24.4%、35.6%、56.2%、57.5% at different concentrations of oxLDL(0、20、40、60、80mg/L) respectively for 24h(P<0.01).HPLC analysis demonstrated the ratios of cellular CE/TC were 10.8%、23.8%、37.0%、55.4%、58.9% at different times of oxLDL(60mg/L) 0h、6h、12h、24h,respectively(P<0.05).
Ⅱ.We found that simvastatin inhibited cxcl16 protein synthesis and lipid accumulation in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner . Oil red O staining showed intracellular lipid droplets were minor with the presence of simvastatin. HPLC analysis demonstrated the ratios of cellular CE/TC were 57.3%、55.1%、46.2%、17.9% at different concerntrations of simvastatin and oxLDL (60mg/L) 0uM、1uM、10uM、100uM ,respectively(P<0.05). HPLC analysis demonstrated the ratios of cellular CE/TC were 57.3%、34.8%、25.9%、17.9% at different times of simvastatin (100uM) and oxLDL (60mg/L) 0h、6h、12h、24h,respectively(P<0.01).
Ⅲ. Western blotting also showed ,there were no significant differences in CXCL16 protein synthesis between the control groups and the lipid-loaded cell groups (CE/TC<50%)(P>0.05).But in the foam cell groups (CE/TC>50%), the CXCL16 protein synthesis was increased . The more lipid droplets was in foam cells ,the more CXCL16 protein synthesis was upregulated.(P<0.05). Western blotting also showed that simvastatin decreased the expression of cxcl16 in a time-dependent and dose-dependent manner (P<0.05).
ConclusionsⅠ.The oxLDL-induced lipid accumulation was in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner.
Ⅱ.Simvastatin may decrease lipid accumulation in murine aortic smooth muscle cells in a time-dependent (incubated with 100umol/L simvastatin from 6 to 24h)and dose-dependent manner(1～100umol/L) .
ⅢSimvastatin may downregulate oxLDL-induced cxcl16 expression in foam cells in a time-dependent((incubated with 100umol/L simvastatin from 6 to 24h)) and dose-dependent manner (1～100umol/L).
方法采用体外培养的SD大鼠平滑肌细胞作为研究对象,换含0.1%血清的培养基培养后加处理因素。
Ⅰ.不同浓度的oxLDL(0、20mg/L、40mg/L、60mg/L、80mg/L)与鼠源平滑肌细胞共同孵育24h和用60mg/L oxLDL与鼠源平滑肌细胞孵育不同时间即(0h、6h、12h、24h、36h),油红O染色观察细胞内脂质蓄积情况,高效液相色谱分析法检测细胞总胆固醇蓄积情况,Western blotting检测平滑肌细胞CXCL16蛋白质的表达。
Ⅱ.用60mg/L oxLDL与不同浓度的辛伐他汀(0uM、1uM、10uM、100uM)共同孵育24h,空白组作为对照组和用60mg/L oxLDL与最佳浓度的辛伐他汀100uM,同时孵育不同的时间即(0h、6h、12h、24h),空白组作为对照组,油红O染色观察细胞内脂质蓄积情况,高效液相色谱分析法检测细胞总胆固醇蓄积情况,Western blotting检测平滑肌细胞CXCL16蛋白质的表达。
结果Ⅰ.oxLDL诱导的鼠源平滑肌细胞脂质蓄积与oxLDL呈剂量依赖性和时间依赖性(P<0.05)。.油红O染色显示:与空白对照组和低浓度组比较,较高浓度的oxLDL组(60mg/L、80mg/L)诱导平滑肌细胞较oxLDL低浓度(20mg/L、40mg/L)组胞内脂滴明显增多,体积增大。oxLDL(60mg/L)较长时间(24h、36h)诱导平滑肌细胞比较短时间(0h、6h、12h)胞内脂滴明显增多,体积增大。在oxLDL浓度为0、20mg/L、40mg/L、60mg/L、80mg/L时,HPLC检测的CE/TC的比值分别为(10.78±1.25)%、(24.40±1.84)%、(35.6±2.47)%、(56.16±1.80)%(P<0.01) (57.50±2.47)%,在60mg/L的oxLDL作用的不同时间即(0h、6h、12h、24h、36h),HPLC检测的CE/TC的比值分别为(10.78±1.25)%、(23.78±1.80)%、(36.95±2.39)%、(55.39±2.22)%、(58.89±4.05)%(P<0.05)。
Ⅱ.辛伐他汀能抑制鼠源平滑肌细胞对oxLDL的摄取,油红O染色可见oxLDL+simvastatin组细胞内脂滴较oxLDL组明显减少,且脂滴颗粒体积变小。在oxLDL(60mg/L)与simvastatin浓度分别为(0uM、1uM、10uM、100uM)时,HPLC检测的CE/TC的比值分别为(57.28±0.83)%、( 55.06±2.05)%、(46.20±1.44)%、( 17.86±0.97)%.正常组的CE/TC的比值为(10.78±1.25)%(P<0.05).在oxLDL(60mg/L)与simvastatin(100uM)作用不同的时间组(0h、6h、12h、24h),HPLC检测的CE/TC的比值分别为(57.28±0.83)%、(34.74±1.21)%、(25.96±1.31)%、(17.86±0.97)%(P<0.01).
Ⅲ.在正常对照组和荷脂细胞(CE/TC<50%)组中,CXCL16蛋白表达无显著差异性(P>0.05),而在泡沫细胞(CE/TC>50%)组中,CXCL16蛋白表达显著增加,CXCL16的表达与细胞泡沫化有关(p<0.05)。辛伐他汀能降低泡沫细胞中的CXCL16的表达,且呈剂量依赖性和时间依赖性(P<0.05)。
结论1. oxLDL诱导鼠源平滑肌细胞脂质蓄积在一定范围内呈剂量依赖性和时间依赖性。
2.辛伐他汀明显降低泡沫细胞内的胆固醇酯与总胆固醇的比值,且在一定范围内呈剂量依赖性和时间依赖性。
3.辛伐他汀能降低泡沫细胞中的CXCL16的表达,且在一定的范围内呈剂量依赖性和时间依赖性。
Objective The purpose of the present study was to investigate the effect of oxLDL(oxidized low-density lipoprotein)-induced lipid accumulation in murine aortic smooth muscle cells, the effect of simvastatin on oxLDL-induced lipid accumulation in foam cells of murine aortic smooth muscle cells and the relation with CXCL16.
MethodsⅠ. Murine Aortic smooth muscle cells were incubated with oxLDL at different concentration (0、20、40、60、80mg/L) respectively for 24h,and murine Aortic smooth muscle cells were incubated with 60mg/L oxLDL at different time (0h、6h、12h、24h、36h).Oil red O staining was used to observe the intracellular lipid droplets.Cellular total cholesterol was determined by high performance liquid chromatography(HPLC) analysis. CXCL16 protein level was determined by Western blotting.
Ⅱ.Murine aortic smooth muscle cells were coincubated with 60mg/L oxLDL and simvastatin at different concentration (0uM、1uM、10uM、100uM) respectively for 24h, and murine aortic smooth muscle cells were coincubated with 60mg/L oxLDL and simvastatin of the best concentration respectively for 0h、6h、12h、24h. murine aortic smooth muscle cells were incubated without oxLDL and simvastatin as the control groups. Oil red O staining was used to observe the intracellular lipid droplets.Cellular total cholesterol was determined by high performance liquid chromatography(HPLC) analysis. CXCL16 protein level was determined by Western blotting.
ResultsⅠ. The oxLDL-induced lipid accumulation was in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner(P<0.05) .Oil red O staining showed the more lipid droplets were in higher concentration oxLDL(60mg/L,80mg/L) groups than lower concentration oxLDL (20mg/L、40mg/L) groups .and the more lipid droplets were in longer time (24h、36h) groups than shorter time(6h、12h) groups. HPLC analysis demonstrated the ratios of cellular CE/TC were 10.8%、24.4%、35.6%、56.2%、57.5% at different concentrations of oxLDL(0、20、40、60、80mg/L) respectively for 24h(P<0.01).HPLC analysis demonstrated the ratios of cellular CE/TC were 10.8%、23.8%、37.0%、55.4%、58.9% at different times of oxLDL(60mg/L) 0h、6h、12h、24h,respectively(P<0.05).
Ⅱ.We found that simvastatin inhibited cxcl16 protein synthesis and lipid accumulation in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner . Oil red O staining showed intracellular lipid droplets were minor with the presence of simvastatin. HPLC analysis demonstrated the ratios of cellular CE/TC were 57.3%、55.1%、46.2%、17.9% at different concerntrations of simvastatin and oxLDL (60mg/L) 0uM、1uM、10uM、100uM ,respectively(P<0.05). HPLC analysis demonstrated the ratios of cellular CE/TC were 57.3%、34.8%、25.9%、17.9% at different times of simvastatin (100uM) and oxLDL (60mg/L) 0h、6h、12h、24h,respectively(P<0.01).
Ⅲ. Western blotting also showed ,there were no significant differences in CXCL16 protein synthesis between the control groups and the lipid-loaded cell groups (CE/TC<50%)(P>0.05).But in the foam cell groups (CE/TC>50%), the CXCL16 protein synthesis was increased . The more lipid droplets was in foam cells ,the more CXCL16 protein synthesis was upregulated.(P<0.05). Western blotting also showed that simvastatin decreased the expression of cxcl16 in a time-dependent and dose-dependent manner (P<0.05).
ConclusionsⅠ.The oxLDL-induced lipid accumulation was in murine aortic smooth muscle cells in a time-dependent and dose-dependent manner.
Ⅱ.Simvastatin may decrease lipid accumulation in murine aortic smooth muscle cells in a time-dependent (incubated with 100umol/L simvastatin from 6 to 24h)and dose-dependent manner(1～100umol/L) .
ⅢSimvastatin may downregulate oxLDL-induced cxcl16 expression in foam cells in a time-dependent((incubated with 100umol/L simvastatin from 6 to 24h)) and dose-dependent manner (1～100umol/L).
引文
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[36].Argmann CA,Edwards JY,Sawyez CG,O Neil,Hegele RA,Pickering JG, Huff MW. Regulation of macrophage cholesterol efflux through HMG-CoA reductase inhibition: A role for RhoA in ABCA1-mediated cholesterol efflux. J Biol Chem 2005;280(23):22212-22221.
[37]. Hitoshi A, Shuichi T, Hisashi Y, et al. Effects of Pravastatin on the Expression of ATP-Binding Cassette ransporter A1[J]. JPET, 2004 ,311(1):420–425.
[1]. Shimaoka T, Kume N, Minami M, Hayashida K, Kataoka H, Kita T, et al. Molecular Cloning of a Novel Scavenger Receptor for Oxidized Low Density Lipoprotein, SR-PSOX, on Macrophages[J]. J. Biol. Chem., 2000; 275: 40663.
[2]. Wilbanks A,Zondlo S C ,Murphy K, Mak S, Soler D, Langdon P, et al. Expression Cloning of the STRL33 /BONZO/TYMSTR Ligand Reveals Elements of CC, CXC, and CX3C Chemokines[J]. J.Immunol., 2001; 166: 5145-5154.
[3]. Chandrasekar B, Bysani S, and Mummidi S. CXCL16 Signals via Gi Phosphatidylinositol 3-Kinase, Akt, I_B Kinase, and Nuclear Factor-_B and Induces Cell-Cell Adhesion and Aortic Smooth Muscle Cell Proliferation[J].J. Biol.Chem. 2004; 279(5): 3188-3196.
[4]. Charo I F, Taubman M B. Chemokines in the Pathogenesis of Vascular Disease. Circ Res. 2004;95:858-866.
[5]. 徐焕宾,熊思东.新发现的CXCL16 趋化因子及其受体《生命的化学》2003 年23卷1期,8-10。
[6]. Gough P J, Garton K J, Wille P T, Rychlewski M, Dempsey P J, and Raines E W. A Disintegrin and Metalloproteinase 10-Mediated Cleavage and Shedding Regulates the Cell Surface Expression of CXC Chemokine Ligand 16[J]. J Immunol,, 2004, 172: 3678–3685.
[7]. Abel S, Hundhausen C, Mentlein R, Schulte A, Berkhout T A., Broadway N,et al. The Transmembrane CXC-Chemokine Ligand 16 Is Induced by IFN- and TNF- and Shed by the Activity of the Disintegrin-Like Metalloproteinase ADAM10[J]. J. Immunol., 2004; 172: 6362 – 6372.
[8]. Shimaoka T, Nakayama T, Hieshima K, Kume N, Fukumoto N, Minami M, et al. Chemokines Generally Exhibit Scavenger Receptor Activity through Their Receptor-binding Domain[J]. J Biol Chem,2004;279(26):26807-26810.
[9]. Hofnagel O, Luechtenborg B, Plenz G, Robenek H. Expression of the novel scavenger receptor SR-PSOX in cultured aortic smooth muscle cells and umbilical endothelial cells[J]. Arterioscler Thromb Vasc Biol. 2002;22:710–711.
[10]. Shashkin P, Simpson D, Mishin V, Chesnutt B, and Ley K. Expression of CXCL16 in Human T Cells[J]. Arterioscler. Thromb. Vasc. Biol., Jan 2003; 23: 148
[11].Matloubian M,.David A, Engel S, Ryan J E, and Cyster J G. A transmembrane CXC chemokine is a ligand for HIV-coreceptor Bonzo[J]. Nat. Immunol.2000; 1:298.
[12]. Johnston B, Kim C H, Soler D, Emoto M., and Butcher E C. Differential chemokine responses and homing patterns of murine TCR__ NKT cell subsets. J. Immunol.2003; 171:2960.
[13]. Bonecchi R, Bianchi G, Bordignon P P, D'Ambrosio D, Lang R, Borsatti A, et al. Differential Expression of Chemokine Receptors and Chemotactic Responsiveness of Type 1 T Helper Cells (Th1s) and Th2s[J] J. Exp. Med., Jan 1998; 187: 129
[14]. Wuttge D M., Zhou Xinghua, Sheikine Y Wagsater D, Stemme V, Hedin U, et al.CXCL16/SR-PSOX Is an Interferon-_–Regulated Chemokine and Scavenger Receptor Expressed in Atherosclerotic Lesions.[J].Arterioscler Thromb Vasc Biol. 2004;24:750-755.
[15].Wagster D,Olofsson PS,Norgren L,Stenberg B,Sirsjo A.The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by interferon gamma.Biochem Biophs Res Commun,2004,325:1187-1193.
[16]. 周 珊 珊 , 郑 杨 .CXCL16 与 动 脉 粥 样 硬 化 .[J]. 中 华 老 年 医 学 杂志,2006,25(6);466-469.
[17].Tenger C, Sundborger A, Jawien J, Zhou Xinghua. IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-_ and CXCL16 Expression Independently of T Cells[J] Arterioscler Thromb Vasc Biol. 2005;25:791-796.
[18].杨永宗,阮长耿,唐朝枢等.动脉粥样硬化性心血管病基础与临床.科学出版社.北京.2004:48-97.
[19]. Minami M, Kume N, Shimaoka T, Kataoka H, Hayashida K, Akiyama Y, et al. Expression of SR-PSOX, a Novel Cell-Surface Scavenger Receptor for Phosphatidylserine and Oxidized LDL in Human Atherosclerotic Lesions[J].Arterioscler Thromb Vasc Biol. 2001;21:1796-1800.
[20]. Aslanian A M., Charo I F, Targeted Disruption of the Scavenger Receptor and Chemokine CXCL16 Accelerates Atherosclerosis[J] Circulation.2006;114:583-590.
[21]. Lundberg GA, Kellin A, Samnegard A, Lundman P, Tornvall P, Dimmeler S,et al.Severity of coronary artery stenosis is associated with a polymorphism in the CXCL16/SR-PSOX gene.[J]J Intern Med, May 1, 2005; 257(5): 415-22.
[22]. Yamauchi R, Tanaka M, Kume N, Minami M, Kawamoto T. Upregulation of SR-PSOX/CXCL16 and Recruitment of CD8+ T Cells in Cardiac Valves During Inflammatory Valvular Heart Disease[J]. Arterioscler. Thromb. Vasc. Biol., Feb 2004; 24: 282.
[23]. Shimaoka T, Nakayama T, Fukumoto N, Kume N, Takahashi S, Yamaguchi J, et al. Cell surface-anchored SR-PSOX/CXC chemokine ligand 16 mediates firmadhesion of CXC chemokine receptor 6-expressing cells[J]J. Leukoc. Biol., Feb 2004;75: 267
[24].Shimaoka T, Nakayama T, Kume N, Takahashi S, Yamaguchi J, Minami M,et al . Cutting Edge: SR-PSOX/CXC Chemokine Ligand 16 Mediates Bacterial Phagocytosis by APCs Through its Chemokine Domain[J]. J. Immunol., Aug 2003; 171: 1647-1651.
[25].Sato T,Thorlacius H,Johnston B,Staton T L,Xiang Wenkai,Littman D R, et al.Role for CXCR6 in Recruitment of Activated CD8_Lymphocytes to Inflamed Liver[J]J.Immunol. 2005,174: 277–283.
[26]. Heydtmann M, Lalor P F, Eksteen J A, Hu¨bscher S G., Briskin M,and Adams D H. CXC Chemokine Ligand 16 Promotes Integrin-Mediated Adhesion of Liver-Infiltrating Lymphocytes to Cholangiocytes and Hepatocytes within the Inflamed Human Liver[J].J. Immunol. 2005,174: 1055–1062.
[27].徐焕宾,龚燕萍,储以微,蒋正刚,熊思东。CXCL16抗体可阻断BCG和LPS诱导的小鼠免疫性肝损伤。中华微生物学和免疫学杂志,2005。25:111-115。
[28]. Fukumoto N, Shimaoka T, Fujimura H, Sakoda S, Tanaka M, Kita T,et al.Critical roles of CXC chemokine ligand 16/scavenger receptor that binds phosphatidylserine and oxidized lipoprotein in the pathogenesis of both acute and adoptive transfer experimental autoimmune encephalomyelitis.[J].J Immunol. 2004,173(3):1620-1627.
[29]. Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N,et al.Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells.[J].J Neurochem. 2005,93(5):1293-1303.
[30]. Wagsater D, Hugander A, Dimberg J. Expression of CXCL16 in human rectal cancer.[J].Int J Mol Med. 2004,14(1):65-69.
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[4]. Hofnagel O, Luechtenborg B, Plenz G, Robenek H. Expression of the novel scavenger receptor SR-PSOX in cultured aortic smooth muscle cells and umbilical endothelial cells[J]. Arterioscler Thromb Vasc Biol. 2002;22:710–711.
[5]. Wilbanks A,Zondlo S C ,Murphy K, Mak S, Soler D, Langdon P, et al. Expression Cloning of the STRL33 /BONZO/TYMSTR Ligand Reveals Elements of CC, CXC, and CX3C Chemokines[J]. J.Immunol.2001; 166: 5145-5154.
[6].Matloubian M,.David A, Engel S, Ryan J E, and Cyster J G. A transmembrane CXC chemokine is a ligand for HIV-coreceptor Bonzo[J]. Nat. Immunol.2000; 1:298-304.
[7]. Chandrasekar B, Bysani S, and Mummidi S. CXCL16 Signals via Gi Phosphatidylinositol 3-Kinase, Akt, I_B Kinase, and Nuclear Factor-_B and Induces Cell-Cell Adhesion and Aortic Smooth Muscle Cell Proliferation[J].J. Biol. Chem. 2004; 279(5): 3188-3196.
[8]. 徐焕宾,熊思东.新发现的CXCL16 趋化因子及其受体《生命的化学》2003 年23卷1期,8-10。
[9]. Aslanian A M., Charo I F, Targeted Disruption of the Scavenger Receptor and Chemokine CXCL16 Accelerates Atherosclerosis[J] Circulation.2006;114:583-590.
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[27].杨永宗,阮长耿,唐朝枢等.动脉粥样硬化性心血管病基础与临床.科学出版社.北京.2004:75-77.
[28]. Shimaoka T, Kume N, Minami M, Hayashida K, Kataoka H, Kita T, et al. Molecular Cloning of a Novel Scavenger Receptor for Oxidized Low Density Lipoprotein, SR-PSOX, on Macrophages[J]. J. Biol. Chem., 2000; 275: 40663
[29]. 杨永宗,阮长耿,唐朝枢等.动脉粥样硬化性心血管病基础与临床.科学出版社.北京.2004:48-97.
[30]. Minami M, Kume N, Shimaoka T, Kataoka H, Hayashida K, Akiyama Y, et al. Expression of SR-PSOX, a Novel Cell-Surface Scavenger Receptor for Phosphatidylserine and Oxidized LDL in Human Atherosclerotic Lesions[J].Arterioscler Thromb Vasc Biol. 2001;21:1796-1800.
[31].Wagster D,Olofsson PS,Norgren L,Stenberg B,Sirsjo A.The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by interferon gamma.Biochem Biophs Res Commun,2004,325:1187-1193.
[32].Chandrasekar B,Mummidi S,Valente AJ, et al.The pro-atherogenic cytokineinterleukin-18 induces CXCL16 expression in rat aortic smooth muscle cells via MyD88,interleukin-1 receptor-associated kinase,tumor necrosis factor receptor-associated factor 6,c-Src, phosphatidylinositol 3-kinase, Akt, c-Jun N-terminal kinase, and activator protein-1 signaling.Biol Chem,2005,280;26263-26277.
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[35].Umetani N,Kanayama Y,Okamura M,Negoro N,Takeda T.Lovastatin inhibits gene expression of type-1 scavenger receptor in THP-1 human macrophages. Biochem Biophys Acta 1996;1303(3):199-206.
[36].Argmann CA,Edwards JY,Sawyez CG,O Neil,Hegele RA,Pickering JG, Huff MW. Regulation of macrophage cholesterol efflux through HMG-CoA reductase inhibition: A role for RhoA in ABCA1-mediated cholesterol efflux. J Biol Chem 2005;280(23):22212-22221.
[37]. Hitoshi A, Shuichi T, Hisashi Y, et al. Effects of Pravastatin on the Expression of ATP-Binding Cassette ransporter A1[J]. JPET, 2004 ,311(1):420–425.
[1]. Shimaoka T, Kume N, Minami M, Hayashida K, Kataoka H, Kita T, et al. Molecular Cloning of a Novel Scavenger Receptor for Oxidized Low Density Lipoprotein, SR-PSOX, on Macrophages[J]. J. Biol. Chem., 2000; 275: 40663.
[2]. Wilbanks A,Zondlo S C ,Murphy K, Mak S, Soler D, Langdon P, et al. Expression Cloning of the STRL33 /BONZO/TYMSTR Ligand Reveals Elements of CC, CXC, and CX3C Chemokines[J]. J.Immunol., 2001; 166: 5145-5154.
[3]. Chandrasekar B, Bysani S, and Mummidi S. CXCL16 Signals via Gi Phosphatidylinositol 3-Kinase, Akt, I_B Kinase, and Nuclear Factor-_B and Induces Cell-Cell Adhesion and Aortic Smooth Muscle Cell Proliferation[J].J. Biol.Chem. 2004; 279(5): 3188-3196.
[4]. Charo I F, Taubman M B. Chemokines in the Pathogenesis of Vascular Disease. Circ Res. 2004;95:858-866.
[5]. 徐焕宾,熊思东.新发现的CXCL16 趋化因子及其受体《生命的化学》2003 年23卷1期,8-10。
[6]. Gough P J, Garton K J, Wille P T, Rychlewski M, Dempsey P J, and Raines E W. A Disintegrin and Metalloproteinase 10-Mediated Cleavage and Shedding Regulates the Cell Surface Expression of CXC Chemokine Ligand 16[J]. J Immunol,, 2004, 172: 3678–3685.
[7]. Abel S, Hundhausen C, Mentlein R, Schulte A, Berkhout T A., Broadway N,et al. The Transmembrane CXC-Chemokine Ligand 16 Is Induced by IFN- and TNF- and Shed by the Activity of the Disintegrin-Like Metalloproteinase ADAM10[J]. J. Immunol., 2004; 172: 6362 – 6372.
[8]. Shimaoka T, Nakayama T, Hieshima K, Kume N, Fukumoto N, Minami M, et al. Chemokines Generally Exhibit Scavenger Receptor Activity through Their Receptor-binding Domain[J]. J Biol Chem,2004;279(26):26807-26810.
[9]. Hofnagel O, Luechtenborg B, Plenz G, Robenek H. Expression of the novel scavenger receptor SR-PSOX in cultured aortic smooth muscle cells and umbilical endothelial cells[J]. Arterioscler Thromb Vasc Biol. 2002;22:710–711.
[10]. Shashkin P, Simpson D, Mishin V, Chesnutt B, and Ley K. Expression of CXCL16 in Human T Cells[J]. Arterioscler. Thromb. Vasc. Biol., Jan 2003; 23: 148
[11].Matloubian M,.David A, Engel S, Ryan J E, and Cyster J G. A transmembrane CXC chemokine is a ligand for HIV-coreceptor Bonzo[J]. Nat. Immunol.2000; 1:298.
[12]. Johnston B, Kim C H, Soler D, Emoto M., and Butcher E C. Differential chemokine responses and homing patterns of murine TCR__ NKT cell subsets. J. Immunol.2003; 171:2960.
[13]. Bonecchi R, Bianchi G, Bordignon P P, D'Ambrosio D, Lang R, Borsatti A, et al. Differential Expression of Chemokine Receptors and Chemotactic Responsiveness of Type 1 T Helper Cells (Th1s) and Th2s[J] J. Exp. Med., Jan 1998; 187: 129
[14]. Wuttge D M., Zhou Xinghua, Sheikine Y Wagsater D, Stemme V, Hedin U, et al.CXCL16/SR-PSOX Is an Interferon-_–Regulated Chemokine and Scavenger Receptor Expressed in Atherosclerotic Lesions.[J].Arterioscler Thromb Vasc Biol. 2004;24:750-755.
[15].Wagster D,Olofsson PS,Norgren L,Stenberg B,Sirsjo A.The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by interferon gamma.Biochem Biophs Res Commun,2004,325:1187-1193.
[16]. 周 珊 珊 , 郑 杨 .CXCL16 与 动 脉 粥 样 硬 化 .[J]. 中 华 老 年 医 学 杂志,2006,25(6);466-469.
[17].Tenger C, Sundborger A, Jawien J, Zhou Xinghua. IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-_ and CXCL16 Expression Independently of T Cells[J] Arterioscler Thromb Vasc Biol. 2005;25:791-796.
[18].杨永宗,阮长耿,唐朝枢等.动脉粥样硬化性心血管病基础与临床.科学出版社.北京.2004:48-97.
[19]. Minami M, Kume N, Shimaoka T, Kataoka H, Hayashida K, Akiyama Y, et al. Expression of SR-PSOX, a Novel Cell-Surface Scavenger Receptor for Phosphatidylserine and Oxidized LDL in Human Atherosclerotic Lesions[J].Arterioscler Thromb Vasc Biol. 2001;21:1796-1800.
[20]. Aslanian A M., Charo I F, Targeted Disruption of the Scavenger Receptor and Chemokine CXCL16 Accelerates Atherosclerosis[J] Circulation.2006;114:583-590.
[21]. Lundberg GA, Kellin A, Samnegard A, Lundman P, Tornvall P, Dimmeler S,et al.Severity of coronary artery stenosis is associated with a polymorphism in the CXCL16/SR-PSOX gene.[J]J Intern Med, May 1, 2005; 257(5): 415-22.
[22]. Yamauchi R, Tanaka M, Kume N, Minami M, Kawamoto T. Upregulation of SR-PSOX/CXCL16 and Recruitment of CD8+ T Cells in Cardiac Valves During Inflammatory Valvular Heart Disease[J]. Arterioscler. Thromb. Vasc. Biol., Feb 2004; 24: 282.
[23]. Shimaoka T, Nakayama T, Fukumoto N, Kume N, Takahashi S, Yamaguchi J, et al. Cell surface-anchored SR-PSOX/CXC chemokine ligand 16 mediates firmadhesion of CXC chemokine receptor 6-expressing cells[J]J. Leukoc. Biol., Feb 2004;75: 267
[24].Shimaoka T, Nakayama T, Kume N, Takahashi S, Yamaguchi J, Minami M,et al . Cutting Edge: SR-PSOX/CXC Chemokine Ligand 16 Mediates Bacterial Phagocytosis by APCs Through its Chemokine Domain[J]. J. Immunol., Aug 2003; 171: 1647-1651.
[25].Sato T,Thorlacius H,Johnston B,Staton T L,Xiang Wenkai,Littman D R, et al.Role for CXCR6 in Recruitment of Activated CD8_Lymphocytes to Inflamed Liver[J]J.Immunol. 2005,174: 277–283.
[26]. Heydtmann M, Lalor P F, Eksteen J A, Hu¨bscher S G., Briskin M,and Adams D H. CXC Chemokine Ligand 16 Promotes Integrin-Mediated Adhesion of Liver-Infiltrating Lymphocytes to Cholangiocytes and Hepatocytes within the Inflamed Human Liver[J].J. Immunol. 2005,174: 1055–1062.
[27].徐焕宾,龚燕萍,储以微,蒋正刚,熊思东。CXCL16抗体可阻断BCG和LPS诱导的小鼠免疫性肝损伤。中华微生物学和免疫学杂志,2005。25:111-115。
[28]. Fukumoto N, Shimaoka T, Fujimura H, Sakoda S, Tanaka M, Kita T,et al.Critical roles of CXC chemokine ligand 16/scavenger receptor that binds phosphatidylserine and oxidized lipoprotein in the pathogenesis of both acute and adoptive transfer experimental autoimmune encephalomyelitis.[J].J Immunol. 2004,173(3):1620-1627.
[29]. Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N,et al.Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells.[J].J Neurochem. 2005,93(5):1293-1303.
[30]. Wagsater D, Hugander A, Dimberg J. Expression of CXCL16 in human rectal cancer.[J].Int J Mol Med. 2004,14(1):65-69.