清道夫受体B族Ⅰ型抑制高价铁诱导的细胞毒性的研究
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摘要
目的
通过观察清道夫受体(Scavenger receptor class B type I, SR-BI)基因敲除小鼠脾脏组织中含铁血黄素的沉积的变化;比较氮基三醋酸铁(ferric nitrilotriacetate, Fe-NTA)诱导的细胞毒性对HepG2(-)细胞SR-BI蛋白表达水平的影响；研究SR-BI蛋白的表达对Fe-NTA、血红蛋白(hemoglobin)或高铁血红素(hemin)等高价铁(Fe3+)诱导的细胞毒性的影响以及探讨Fe-NTA诱导细胞毒性的发生机制,为SR-BI可以抑制Fe-NTA、Fe-NTA-H2O2、hemoglobin-H2O2和hemin-H2O2等高价铁(Fe3+)所诱导的细胞毒性提供一定的理论和实验依据,为SR-BI功能研究提供新的关注点。
方法
1.SR-BI杂合子(SR-BI+/-)小鼠交配繁殖,筛选SR-BI正常和SR-BI基因敲除小鼠,8-12周龄小鼠麻醉处死,分离摘取脾脏组织,常规组织切片、HE染色和普鲁士蓝染色,显微镜下观察比较两组小鼠脾脏组织结构、脾脏红髓中含铁血黄素(haemosiderin)沉积量的变化。
2.采用蛋白质印迹(Western blot)技术检测不同浓度Fe-NTA培养的人肝癌HepG2(-)细胞中SR-BI蛋白表达的变化；利用细胞转染技术将human-SR-BI-cDNA转染中国仓鼠卵巢(CHO)细胞,筛选建立CHO-SR-BI和CHO-Vector细胞株。选取2-3代的培养细胞,分别单独给予浓度都为0、0.2、0.4、0.8、1.0mM的Fe-NTA、H2O2,浓度为0、0.8、1.0、2.0mM的NTA,显微镜下观察细胞生长状态的变化,检测细胞培养基中乳酸脱氢酶(lactate dehydrogenase, LDH)的含量,探讨SR-BI蛋白的表达对Fe-NTA诱导的细胞毒性的影响以及NTA、H2O2对细胞生长的影响。
3.选取2-3代培养的CHO-SR-BI细胞和CHO-Vector细胞,分别给予0.2mM Fe-NTA培养24小时和0.05mM Fe-NTA培养48小时,显微镜下观察细胞生长状态变化,提取细胞DNA,利用琼脂糖凝胶电泳DNA鉴定技术,检测有无DNA梯状条带的形成,探讨Fe-NTA诱导的细胞毒性的发生机制；分别给予浓度为0、0.2、0.4、0.8、1.0mM的Fe-NTA-H2O2,浓度为0、6.25、12.5、25.0uM血红蛋白-H2O2、高铁血红素-H2O2,显微镜下观察细胞生长状态的变化,检测CHO-SR-BI细胞和CHO-Vector细胞的培养基中LDH的含量,比较SR-BI蛋白的表达对上述各种含高价铁(Fe3+)混合物所诱导的细胞毒性的影响。
结果
1.HE染色和普鲁士蓝染色：与SR-BI正常小鼠相比,SR-BI基因敲除小鼠脾脏红髓、白髓分布不规律,红白髓界限不清,白髓大小不一,尤其是红髓区域内出现大量含铁血黄素的沉积(p<0.05)
2.在本实验条件下,实验结果表明Fe-NTA可以诱导细胞出现非凋亡性的损伤和死亡；蛋白印迹技术检测结果显示Fe-NTA诱导的细胞毒性对HepG2(-)细胞中SR-BI蛋白表达水平没有明显影响(p>0.05)。
3.H2O2对于Fe-NTA诱导的细胞毒性有明显的增强作用(p<0.05)；给予不同浓度的Fe-NTA、Fe-NTA-H2O2、血红蛋白-H2O2及高铁血红素-H2O2培养后,CHO-SR-BI细胞培养基中LDH释放百分比例显著低于CHO-Vector细胞组,两组的差异具有统计学意义(p<0.05),说明细胞中SR-BI蛋白的表达可以明显抑制Fe-NTA、Fe-NTA-H2O2、血红蛋白-H2O2、高铁血红素-H2O2等含高价铁(Fe3+)的混合物所诱导的细胞毒性。。
结论
1.SR-BI基因敲除小鼠脾脏红髓、白髓分布不规律,红白髓界限不清,白髓大小不一,尤其是红髓区域内出现大量含铁血黄素的沉积。
2. Fe-NTA诱导浓度依赖性的细胞毒性,并导致细胞出现非凋亡性的损伤和死亡,而Fe-NTA对HepG2(-)细胞中SR-BI蛋白的表达并没有明显影响。
3.H2O2明显增强Fe-NTA诱导的细胞毒性；SR-BI不仅明显抑制Fe-NTA诱导的细胞毒性,而且显著抑制Fe-NTA-H2O2、血红蛋白-H2O2、高铁血红素-H2O2等含高价铁(Fe3+)的混合物所诱导的细胞毒性。
OBJECTIVE
To evaluate the histological changes and iron deposition in the Red Pulp of spleens of SR-BI-deficient mice, effects of Fe-NTA on SR-BI expression in HepG2(-) cells and effects of SR-BI on suppression of cytotoxicity-induced by trivalent iron, such as Fe-NTA, hemoglobin or hemin. Furthermore, explore the underlying mechanism of the cell damage and death induced by Fe-NTA, so to provide a theoretical and experimental evidence of SR-BI suppresses cytotoxicity-induced by trivalent iron and a new focus on the function of SR-BI research.
METHODS
1. Heterozygous SR-BI+/- mice on a mixed C57BL/6 x129-background were obtained from the Jackson Laboratory. SR-BI-/- and SR-BI+/+ littermates were generated by mating SR-BI+/- mice.8-12 week-old mice were sacrificed by anesthesia. Spleens were isolated and removed for the conventional tissue sections and HE and Perls Prussian Blue staining. Evaluate the histological changes and hemosiderin deposition in the Red Pulp of spleens of SR-BI+/+ and SR-BI-/- mice under microscope.
2. Using Western blot to detect the expression levels of SR-BI in HepG2 (-) cells that treated by various concentrations of Fe-NTA; transfect the human SR-BI-cDNA into CHO cells to generate CHO-Vector cells and CHO-SR-BI cells, then 2- to 3-generations used in experiments were treated with different concentrations of Fe-NTA (0,0.2,0.4,0.8 and 1.0mM), NTA (0,0.8,1.0 and 2.0mM) and H2O2 (0,0.2,0.4 0.8 and 1.0mM). Assess the cells ability by microscope, detect the LDH levels in the cultured cells medium and the effects of SR-BI on the cytotoxicity induced by Fe-NTA.
3.2- to 3-generations of CHO-SR-BI cells and CHO-Vector cells were treated with0.2 mM Fe-NTA for 24 hours and 0.05mM Fe-NTA for 48 hours. Assess the cells ability using the microscope, extract cells DNA and identificate DNA ladder of the cell apoptosis by using DNA agarose gel electrophoresis to explore the underlying mechanism of cytotoxicity induced by Fe-NTA.2- to 3-generations of cultured CHO-SR-BI cells and CHO-Vector cells were treated with different concentrations of Fe-NTA-H2O2 complexes (0,0.2,0.4,0.8 and 1.0mM), hemoglobin-H202 complexes (0,6.25,12.5 and 25.0uM) and hemin-H2O2 complexes (0,6.25,12.5 and 25.0uM). Assess the cells ability using the microscope, detect the LDH levels in the two cultured cells medium and the effects of the expression of SR-BI on cytotoxicities induced by complexes used in our experiments.
RESULTS
1. HE and Perls Prussian Blue staining:Compared to SR-BI+/+ littermates, the histological structure of SR-BI-/- mice was changed, the distribution of red pulp and the various size of white pulp is irregular, and the amount of hemosiderin and the content of iron in the red pulp region of spleens of SR-BI-/- mice were significantly increased.
2. In our experimental conditions, the results indicated that Fe-NTA could result in the non-apoptotic cell damage and death. Western blot detection and assay:There was no obviously up-regulation expression of SR-BI of the human HepG2 (-) cells under the various concentrations of Fe-NTA (p>0.05)
3. Cytotoxicity-induced by Fe-NTA was markly enhanced by H2O2 (p<0.05); compared to control groups (CHO-Vector cells), the LDH release percents were obviously lower in the experiment groups (CHO-SR-BI) in the different concentrations of Fe-NTA, Fe-NTA and H2O2 complexes, hemoglobin and H2O2 complexes or hemin and H2O2 complexes, there is significant difference of the percent between control groups and experiment groups (p<0.05).
CONCLUSION
1. Compared to SR-BI+/+ littermates, the histological structure of SR-BI-/- mice was changed, the distribution of red pulp and the various size of white pulp is irregular, and the amount of hemosiderin and the content of iron in the red pulp region of spleens of SR-BI-/-mice were significantly increased.
2. Cytotoxicity induced by Fe-NTA is in a dose-dependent way to result in the non-apoptotic cell damage and death in our experimental conditions. There were no significant changes of SR-BI expression levels in HepG2 (-) cells treated by various concentrations of Fe-NTA.
3. Cytotoxicity induced by Fe-NTA was markly enhanced by H2O2 SR-BI suppresses cytotoxicity-induced by trivalent iron, such as Fe-NTA, Fe-NTA-H2O2 complexes, hemoglobin-H2O2 complexes or hemin-H2O2 complexes.
通过观察清道夫受体(Scavenger receptor class B type I, SR-BI)基因敲除小鼠脾脏组织中含铁血黄素的沉积的变化;比较氮基三醋酸铁(ferric nitrilotriacetate, Fe-NTA)诱导的细胞毒性对HepG2(-)细胞SR-BI蛋白表达水平的影响；研究SR-BI蛋白的表达对Fe-NTA、血红蛋白(hemoglobin)或高铁血红素(hemin)等高价铁(Fe3+)诱导的细胞毒性的影响以及探讨Fe-NTA诱导细胞毒性的发生机制,为SR-BI可以抑制Fe-NTA、Fe-NTA-H2O2、hemoglobin-H2O2和hemin-H2O2等高价铁(Fe3+)所诱导的细胞毒性提供一定的理论和实验依据,为SR-BI功能研究提供新的关注点。
方法
1.SR-BI杂合子(SR-BI+/-)小鼠交配繁殖,筛选SR-BI正常和SR-BI基因敲除小鼠,8-12周龄小鼠麻醉处死,分离摘取脾脏组织,常规组织切片、HE染色和普鲁士蓝染色,显微镜下观察比较两组小鼠脾脏组织结构、脾脏红髓中含铁血黄素(haemosiderin)沉积量的变化。
2.采用蛋白质印迹(Western blot)技术检测不同浓度Fe-NTA培养的人肝癌HepG2(-)细胞中SR-BI蛋白表达的变化；利用细胞转染技术将human-SR-BI-cDNA转染中国仓鼠卵巢(CHO)细胞,筛选建立CHO-SR-BI和CHO-Vector细胞株。选取2-3代的培养细胞,分别单独给予浓度都为0、0.2、0.4、0.8、1.0mM的Fe-NTA、H2O2,浓度为0、0.8、1.0、2.0mM的NTA,显微镜下观察细胞生长状态的变化,检测细胞培养基中乳酸脱氢酶(lactate dehydrogenase, LDH)的含量,探讨SR-BI蛋白的表达对Fe-NTA诱导的细胞毒性的影响以及NTA、H2O2对细胞生长的影响。
3.选取2-3代培养的CHO-SR-BI细胞和CHO-Vector细胞,分别给予0.2mM Fe-NTA培养24小时和0.05mM Fe-NTA培养48小时,显微镜下观察细胞生长状态变化,提取细胞DNA,利用琼脂糖凝胶电泳DNA鉴定技术,检测有无DNA梯状条带的形成,探讨Fe-NTA诱导的细胞毒性的发生机制；分别给予浓度为0、0.2、0.4、0.8、1.0mM的Fe-NTA-H2O2,浓度为0、6.25、12.5、25.0uM血红蛋白-H2O2、高铁血红素-H2O2,显微镜下观察细胞生长状态的变化,检测CHO-SR-BI细胞和CHO-Vector细胞的培养基中LDH的含量,比较SR-BI蛋白的表达对上述各种含高价铁(Fe3+)混合物所诱导的细胞毒性的影响。
结果
1.HE染色和普鲁士蓝染色：与SR-BI正常小鼠相比,SR-BI基因敲除小鼠脾脏红髓、白髓分布不规律,红白髓界限不清,白髓大小不一,尤其是红髓区域内出现大量含铁血黄素的沉积(p<0.05)
2.在本实验条件下,实验结果表明Fe-NTA可以诱导细胞出现非凋亡性的损伤和死亡；蛋白印迹技术检测结果显示Fe-NTA诱导的细胞毒性对HepG2(-)细胞中SR-BI蛋白表达水平没有明显影响(p>0.05)。
3.H2O2对于Fe-NTA诱导的细胞毒性有明显的增强作用(p<0.05)；给予不同浓度的Fe-NTA、Fe-NTA-H2O2、血红蛋白-H2O2及高铁血红素-H2O2培养后,CHO-SR-BI细胞培养基中LDH释放百分比例显著低于CHO-Vector细胞组,两组的差异具有统计学意义(p<0.05),说明细胞中SR-BI蛋白的表达可以明显抑制Fe-NTA、Fe-NTA-H2O2、血红蛋白-H2O2、高铁血红素-H2O2等含高价铁(Fe3+)的混合物所诱导的细胞毒性。。
结论
1.SR-BI基因敲除小鼠脾脏红髓、白髓分布不规律,红白髓界限不清,白髓大小不一,尤其是红髓区域内出现大量含铁血黄素的沉积。
2. Fe-NTA诱导浓度依赖性的细胞毒性,并导致细胞出现非凋亡性的损伤和死亡,而Fe-NTA对HepG2(-)细胞中SR-BI蛋白的表达并没有明显影响。
3.H2O2明显增强Fe-NTA诱导的细胞毒性；SR-BI不仅明显抑制Fe-NTA诱导的细胞毒性,而且显著抑制Fe-NTA-H2O2、血红蛋白-H2O2、高铁血红素-H2O2等含高价铁(Fe3+)的混合物所诱导的细胞毒性。
OBJECTIVE
To evaluate the histological changes and iron deposition in the Red Pulp of spleens of SR-BI-deficient mice, effects of Fe-NTA on SR-BI expression in HepG2(-) cells and effects of SR-BI on suppression of cytotoxicity-induced by trivalent iron, such as Fe-NTA, hemoglobin or hemin. Furthermore, explore the underlying mechanism of the cell damage and death induced by Fe-NTA, so to provide a theoretical and experimental evidence of SR-BI suppresses cytotoxicity-induced by trivalent iron and a new focus on the function of SR-BI research.
METHODS
1. Heterozygous SR-BI+/- mice on a mixed C57BL/6 x129-background were obtained from the Jackson Laboratory. SR-BI-/- and SR-BI+/+ littermates were generated by mating SR-BI+/- mice.8-12 week-old mice were sacrificed by anesthesia. Spleens were isolated and removed for the conventional tissue sections and HE and Perls Prussian Blue staining. Evaluate the histological changes and hemosiderin deposition in the Red Pulp of spleens of SR-BI+/+ and SR-BI-/- mice under microscope.
2. Using Western blot to detect the expression levels of SR-BI in HepG2 (-) cells that treated by various concentrations of Fe-NTA; transfect the human SR-BI-cDNA into CHO cells to generate CHO-Vector cells and CHO-SR-BI cells, then 2- to 3-generations used in experiments were treated with different concentrations of Fe-NTA (0,0.2,0.4,0.8 and 1.0mM), NTA (0,0.8,1.0 and 2.0mM) and H2O2 (0,0.2,0.4 0.8 and 1.0mM). Assess the cells ability by microscope, detect the LDH levels in the cultured cells medium and the effects of SR-BI on the cytotoxicity induced by Fe-NTA.
3.2- to 3-generations of CHO-SR-BI cells and CHO-Vector cells were treated with0.2 mM Fe-NTA for 24 hours and 0.05mM Fe-NTA for 48 hours. Assess the cells ability using the microscope, extract cells DNA and identificate DNA ladder of the cell apoptosis by using DNA agarose gel electrophoresis to explore the underlying mechanism of cytotoxicity induced by Fe-NTA.2- to 3-generations of cultured CHO-SR-BI cells and CHO-Vector cells were treated with different concentrations of Fe-NTA-H2O2 complexes (0,0.2,0.4,0.8 and 1.0mM), hemoglobin-H202 complexes (0,6.25,12.5 and 25.0uM) and hemin-H2O2 complexes (0,6.25,12.5 and 25.0uM). Assess the cells ability using the microscope, detect the LDH levels in the two cultured cells medium and the effects of the expression of SR-BI on cytotoxicities induced by complexes used in our experiments.
RESULTS
1. HE and Perls Prussian Blue staining:Compared to SR-BI+/+ littermates, the histological structure of SR-BI-/- mice was changed, the distribution of red pulp and the various size of white pulp is irregular, and the amount of hemosiderin and the content of iron in the red pulp region of spleens of SR-BI-/- mice were significantly increased.
2. In our experimental conditions, the results indicated that Fe-NTA could result in the non-apoptotic cell damage and death. Western blot detection and assay:There was no obviously up-regulation expression of SR-BI of the human HepG2 (-) cells under the various concentrations of Fe-NTA (p>0.05)
3. Cytotoxicity-induced by Fe-NTA was markly enhanced by H2O2 (p<0.05); compared to control groups (CHO-Vector cells), the LDH release percents were obviously lower in the experiment groups (CHO-SR-BI) in the different concentrations of Fe-NTA, Fe-NTA and H2O2 complexes, hemoglobin and H2O2 complexes or hemin and H2O2 complexes, there is significant difference of the percent between control groups and experiment groups (p<0.05).
CONCLUSION
1. Compared to SR-BI+/+ littermates, the histological structure of SR-BI-/- mice was changed, the distribution of red pulp and the various size of white pulp is irregular, and the amount of hemosiderin and the content of iron in the red pulp region of spleens of SR-BI-/-mice were significantly increased.
2. Cytotoxicity induced by Fe-NTA is in a dose-dependent way to result in the non-apoptotic cell damage and death in our experimental conditions. There were no significant changes of SR-BI expression levels in HepG2 (-) cells treated by various concentrations of Fe-NTA.
3. Cytotoxicity induced by Fe-NTA was markly enhanced by H2O2 SR-BI suppresses cytotoxicity-induced by trivalent iron, such as Fe-NTA, Fe-NTA-H2O2 complexes, hemoglobin-H2O2 complexes or hemin-H2O2 complexes.
引文
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[26]Glei M, Klenow S, Sauer J, et al, Hemoglobin and hemin induce DNA damage in human colon tumor cells HT29 clone 19A and in primary human colonocytes[J]. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis,2006 Feb 22; 594(1-2):162-171.
[27]Acton S, Rigotti A, Landschulz KT, et al, Identification of scavenger receptor SR-BI as a high density lipoprotein receptor[J]. Science.1996.271(5248):518-520.
[28]Li XA, Titlow WB, Jackson BA, et al, High Density Lipoprotein Binding to Scavenger Receptor, Class B, Type I Activates Endothelial Nitric-oxide Synthase in a Ceramide-dependent Manner[J]. J. Biol. Chem.2002 Mar.277(13):11058-11063.
[29]Tseng MT, Dozier A, Haribabu B, et al, Transendothelial migration of ferric ion in FeCl3 injured murine common carotid artery[J]. Thrombosis Research.2006.118(2):275-280.
[30]Li XA, Guo L, Dressman JL, et al, A Novel Ligand-independent Apoptotic Pathway Induced by Scavenger Receptor Class B, Type I and Suppressed by Endothelial Nitric-oxide Synthase and High Density Lipoprotein[J]. J. Biol. Chem.2005 May.280(19): 19087-19096.
[31]Sakurai, K. and A.I. Cederbaum, Oxidative Stress and Cytotoxicity Induced by Ferric-Nitrilotriacetate in HepG2 Cells That Express Cytochrome P450 2E1[J]. Mol Pharmacol.1998 Dec.54(6):1024-1035.
[32]Giulivi C, Hochestein P, Davies KJ, et al, Hydrogen peroxide production by red blood cells[J]. Free Radic Biol Med 1994 Jan.16(1):123-129.
[33]Naqui A, Chance B, Cadenas E, et al, Reactive Oxygen Intermediates in Biochemistry[J]. Annual Review of Biochemistry.1986.55(1):137-166.
[34]D'Agnillo F, Alayash AI, Interactions of hemoglobin with hydrogen peroxide alters thiol levels and course of endothelial cell death[J]. Am J Physiol Heart Circ Physiol.2000 Oct.279(4):H1880-1889.
[35]Everse J, Hsia N, The Toxicities of Native and Modified Hemoglobins[J]. Free Radic Biol Med.1997.22(6):1075-1099.
[1]Gwynne JT, S.J.r, The role of lipoproteins in steroidogenesis and cholesterol metabolism in steroidogenic glands[J]. Endocr Rev;1982.3(3):299-329.
[2]Krieger, M, Charting the fate of the "Good Cholesterol":Identification and Character-ization of the High-Density Lipoprotein Receptor SR-BI[J]. Annual Review of Biochemi-stry,1999.68(1):523-558.
[3]Webb N, de Villiers WJ, Connell PM, et al, Alternative forms of the scavenger receptor BI (SR-BI) [J]. J. Lipid Res.,1997.38(7):1490-1495.
[4]Webb N.R, Connell PM, Graf GA, et al, SR-BII, an Isoform of the Scavenger Receptor BI Containing an Alternate Cytoplasmic Tail, Mediates Lipid Transfer between High Density Lipoprotein and Cells[J]. Journal of Biological Chemistry,1998.273(24):15241-15248.
[5]Vinals M, Xu S, Vasile E, et al, Identification of the N-Linked Glycosylation Sites on the High Density Lipoprotein (HDL) Receptor SR-BI and Assessment of Their Effects on HDL Binding and Selective Lipid Uptake[J]. J. Biol. Chem.,2003.278(7):5325-5332.
[6]Reaven E, Nomoto A, Leers-Sucheta S, et al, Expression and microvillar localization of scavenger receptor, class B, type I (a high density lipoprotein receptor) in luteinized and hormone-desensitized rat ovarian models[J]. Endocrinology,1998.139:2847-2856.
[7]Reaven, E, Zhan L, Nomoto A, et al, Expression and microvillar localization of scavenger receptor class B, type I (SR-BI) and selective cholesteryl ester uptake in Leydig cells from rat testis[J]. J Lipid Res,2000.41:343-356.
[8]Rigotti A, Edelman ER, Seifert P, et al, Regulation by Adrenocorticotropic Hormone of the in Vivo Expression of Scavenger Receptor Class B Type I (SR-BI), a High Density Lipoprotein Receptor, in Steroidogenic Cells of the Murine Adrenal Gland[J]. J. Biol. Chem.,1996.271(52):33545-33549.
[9]Cao G, Garcia CK, Wyne KL, et al, Structure and Localization of the Human Gene Encoding SR-BI/CLA-1[J]. Journal of Biological Chemistry,1997.272(52):33068-33076.
[10]Duncan K.G, Hosseini K, Bailey KR, et al, Expression of reverse cholesterol transport proteins ATP-binding cassette A1 (ABCA1) and scavenger receptor BI (SR-BI) in the retina and retinal pigment epithelium[J]. British Journal of Ophthalmology,2009.93(8): 1116-1120.
[11]Azhar, S. and E. Reaven, Scavenger receptor class BI and selective cholesteryl ester uptake:partners in the regulation of steroidogenesis[J]. Mol Cell Endocrinol,2002 Sep. 195(1-2):1-26.
[12]Wiersma H, Nijstad N, Gautier T, et al, Scavenger receptor BI (SR-BI) facilitates hepatic very low density lipoprotein (VLDL) production in mice[J]. J. Lipid Res,2010 Mar:51(3):544-553.
[13]Calvo D,_Gomez-Coronado D, Lasuncion MA, et al, CLA-1 Is an 85-kD Plasma Membrane Glycoprotein That Acts as a High-Affinity Receptor for Both Native (HDL, LDL, and VLDL) and Modified (OxLDL and AcLDL) Lipoproteins[J]. Arterioscler Thromb Vasc Biol,1997.17(11):2341-2349.
[14]Gu X, K. Kozarsky, and M. Krieger, Scavenger Receptor Class B, Type I-mediated [3H]Cholesterol Efflux to High and Low Density Lipoproteins Is Dependent on Lipoprotein Binding to the Receptor[J]. J. Biol. Chem.,2000.275(39):29993-30001.
[15]Williams D.L, J.S. Wong, et al, SR-BI is required for microvillar channel formation and the localization of HDL particles to the surface of adrenocortical cells in vivo[J]. J. Lipid Res.,2002.43(4):544-549.
[16]Li X.-A, Titlow WB, Jackson BA, et al, High Density Lipoprotein Binding to Scavenger Receptor, Class B, Type I Activates Endothelial Nitric-oxide Synthase in a Ceramide-dependent Manner[J]. J. Biol. Chem.,2002.277(13):11058-11063.
[17]Miyazaki A, N.H., Horiuchi S, Scavenger receptors that recognize advanced glycation end products[J]. Trends Cardiovasc Med,2002 Aug.12(6):258-262.
[18]Li X.-A, Guo L, Dressman JL, et al, A Novel Ligand-independent Apoptotic Pathway Induced by Scavenger Receptor Class B, Type I and Suppressed by Endothelial Nitric-oxide Synthase and High Density Lipoprotein[J]. J. Biol. Chem.,2005.280(19):19087-19096.
[19]Barba G., Harper F, Harada T, et al, Hepatitis C virus core protein shows a cytoplasmic localization and associates to cellular lipid storage droplets[J]. Proceedings of the National Academy of Sciences of the United States of America,1997.94(4):1200-1205.
[20]Kawasaki Y., Nakagawa A, Nagaosa K, et al, Phosphatidylserine Binding of Class B Scavenger Receptor Type I, a Phagocytosis Receptor of Testicular Sertoli Cells[J]. Journal of Biological Chemistry,2002.277(30):27559-27566.
[21]Azhar S, A. Nomoto and E. Reaven, Hormonal regulation of adrenal microvillar channel formation[J]. J Lipid Res,2002.43:861-871.
[22]Acton, S, Scherer PE, Lodish HF, et al, Expression cloning of SR-BI, a CD36-related class B scavenger receptor[J]. J. Biol. Chem.,1994.269(33):21003-21009.
[23]Temel R, Trigatti B, DeMattos RB, et al, Scavenger receptor class B, type I (SR-BI) is the major route for the delivery of high density lipoprotein cholesterol to the steroidogenic pathway in cultured mouse adrenocortical cells[J]. Proc Natl Acad Sci USA,1997.94:13600-13605.
[24]Rigotti A T.B., Babitt J, et al. Scavenger receptor BI--a cell surface receptor for high density lipoprotein[J]. CUrrent Opinion in Lipidology,1997.8(3):181-188.
[25]Mardones P, Quinones V, Amigo L, et al, Hepatic cholesterol and bile acid metabolism and intestinal cholesterol absorption in scavenger receptor class B type I-deficient mice[J]. J. Lipid Res.,2001.42(2):170-180.
[26]Varban M.L., Rinninger Franz, Wang nang, et al, Targeted mutation reveals a central role for SR-BI in hepatic selective uptake of high density lipoprotein cholesterol[J]. Proceedings of the National Academy of Sciences of the United States of America,1998. 95(8):4619-4624.
[27]Kozarsky K.F, Donahee MH, Glick JM, et al, Gene Transfer and Hepatic Overexpres-sion of the HDL Receptor SR-BI Reduces Atherosclerosis in the Cholesterol-Fed LDL Receptor-Deficient Mouse[J]. Arterioscler Thromb Vasc Biol,2000.20(3):721-727.
[28]Wang N, Arai T. Ji Y, et al, Liver-specific Overexpression of Scavenger Receptor BI Decreases Levels of Very Low Density Lipoprotein ApoB, Low Density Lipoprotein ApoB, and High Density Lipoprotein in Transgenic Mice[J]. J. Biol. Chem.,1998. 273(49):32920-32926.
[29]Ueda Y, Royer L, Gong E, et al, Lower Plasma Levels and Accelerated Clearance of High Density Lipoprotein (HDL) and Non-HDL Cholesterol in Scavenger Receptor Class B Type I Transgenic Mice[J]. J. Biol. Chem.,1999.274(11):7165-7171.
[30]Swarnakar S, Temel RE, Connelly MA, et al, Scavenger Receptor Class B, Type I, Mediates Selective Uptake of Low Density Lipoprotein Cholesteryl Ester[J]. Journal of Biological Chemistry,1999.274(42):29733-29739.
[31]Thuahnai S.T, Lund-Katz S, Willimas DL, et al, Scavenger Receptor Class B, Type I-mediated Uptake of Various Lipids into Cells[J]. Journal of Biological Chemistry,2001. 276(47):43801-43808.
[32]Greene D.J, J.W. Skeggs, and R.E. Morton. Elevated Triglyceride Content Diminishes the Capacity of High Density Lipoprotein to Deliver Cholesteryl Esters via the Scavenger Receptor Class B Type I (SR-BI) [J]. Journal of Biological Chemistry,2001. 276(7):4804-4811.
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[38]Guo L, Song Z, Li M, et al, Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response[J]. Journal of Biological Chemistry,2009.284(30):19826-19834.
[39]Dole V.S, Matuskova J, Vasile E, et al, Thrombocytopenia and Platelet Abnormalities in High-Density Lipoprotein Receptor-Deficient Mice[J]. Arterioscler Thromb Vasc Biol,2008.28(6):1111-1116.
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[12]Meurs I, Hoekstra M, van Wanrooij EJ, et al, HDL cholesterol levels are an important factor for determining the lifespan of erythrocytes[J]. Experimental hematology,2005 Nov.33(11):1309-1319
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[17]Guo L, Song Z, Wu Q, et al, Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response[J]. Journal of Biological Chemistry.2009 Jul.284(30):19826-19834.
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[26]Glei M, Klenow S, Sauer J, et al, Hemoglobin and hemin induce DNA damage in human colon tumor cells HT29 clone 19A and in primary human colonocytes[J]. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis,2006 Feb 22; 594(1-2):162-171.
[27]Acton S, Rigotti A, Landschulz KT, et al, Identification of scavenger receptor SR-BI as a high density lipoprotein receptor[J]. Science.1996.271(5248):518-520.
[28]Li XA, Titlow WB, Jackson BA, et al, High Density Lipoprotein Binding to Scavenger Receptor, Class B, Type I Activates Endothelial Nitric-oxide Synthase in a Ceramide-dependent Manner[J]. J. Biol. Chem.2002 Mar.277(13):11058-11063.
[29]Tseng MT, Dozier A, Haribabu B, et al, Transendothelial migration of ferric ion in FeCl3 injured murine common carotid artery[J]. Thrombosis Research.2006.118(2):275-280.
[30]Li XA, Guo L, Dressman JL, et al, A Novel Ligand-independent Apoptotic Pathway Induced by Scavenger Receptor Class B, Type I and Suppressed by Endothelial Nitric-oxide Synthase and High Density Lipoprotein[J]. J. Biol. Chem.2005 May.280(19): 19087-19096.
[31]Sakurai, K. and A.I. Cederbaum, Oxidative Stress and Cytotoxicity Induced by Ferric-Nitrilotriacetate in HepG2 Cells That Express Cytochrome P450 2E1[J]. Mol Pharmacol.1998 Dec.54(6):1024-1035.
[32]Giulivi C, Hochestein P, Davies KJ, et al, Hydrogen peroxide production by red blood cells[J]. Free Radic Biol Med 1994 Jan.16(1):123-129.
[33]Naqui A, Chance B, Cadenas E, et al, Reactive Oxygen Intermediates in Biochemistry[J]. Annual Review of Biochemistry.1986.55(1):137-166.
[34]D'Agnillo F, Alayash AI, Interactions of hemoglobin with hydrogen peroxide alters thiol levels and course of endothelial cell death[J]. Am J Physiol Heart Circ Physiol.2000 Oct.279(4):H1880-1889.
[35]Everse J, Hsia N, The Toxicities of Native and Modified Hemoglobins[J]. Free Radic Biol Med.1997.22(6):1075-1099.
[1]Gwynne JT, S.J.r, The role of lipoproteins in steroidogenesis and cholesterol metabolism in steroidogenic glands[J]. Endocr Rev;1982.3(3):299-329.
[2]Krieger, M, Charting the fate of the "Good Cholesterol":Identification and Character-ization of the High-Density Lipoprotein Receptor SR-BI[J]. Annual Review of Biochemi-stry,1999.68(1):523-558.
[3]Webb N, de Villiers WJ, Connell PM, et al, Alternative forms of the scavenger receptor BI (SR-BI) [J]. J. Lipid Res.,1997.38(7):1490-1495.
[4]Webb N.R, Connell PM, Graf GA, et al, SR-BII, an Isoform of the Scavenger Receptor BI Containing an Alternate Cytoplasmic Tail, Mediates Lipid Transfer between High Density Lipoprotein and Cells[J]. Journal of Biological Chemistry,1998.273(24):15241-15248.
[5]Vinals M, Xu S, Vasile E, et al, Identification of the N-Linked Glycosylation Sites on the High Density Lipoprotein (HDL) Receptor SR-BI and Assessment of Their Effects on HDL Binding and Selective Lipid Uptake[J]. J. Biol. Chem.,2003.278(7):5325-5332.
[6]Reaven E, Nomoto A, Leers-Sucheta S, et al, Expression and microvillar localization of scavenger receptor, class B, type I (a high density lipoprotein receptor) in luteinized and hormone-desensitized rat ovarian models[J]. Endocrinology,1998.139:2847-2856.
[7]Reaven, E, Zhan L, Nomoto A, et al, Expression and microvillar localization of scavenger receptor class B, type I (SR-BI) and selective cholesteryl ester uptake in Leydig cells from rat testis[J]. J Lipid Res,2000.41:343-356.
[8]Rigotti A, Edelman ER, Seifert P, et al, Regulation by Adrenocorticotropic Hormone of the in Vivo Expression of Scavenger Receptor Class B Type I (SR-BI), a High Density Lipoprotein Receptor, in Steroidogenic Cells of the Murine Adrenal Gland[J]. J. Biol. Chem.,1996.271(52):33545-33549.
[9]Cao G, Garcia CK, Wyne KL, et al, Structure and Localization of the Human Gene Encoding SR-BI/CLA-1[J]. Journal of Biological Chemistry,1997.272(52):33068-33076.
[10]Duncan K.G, Hosseini K, Bailey KR, et al, Expression of reverse cholesterol transport proteins ATP-binding cassette A1 (ABCA1) and scavenger receptor BI (SR-BI) in the retina and retinal pigment epithelium[J]. British Journal of Ophthalmology,2009.93(8): 1116-1120.
[11]Azhar, S. and E. Reaven, Scavenger receptor class BI and selective cholesteryl ester uptake:partners in the regulation of steroidogenesis[J]. Mol Cell Endocrinol,2002 Sep. 195(1-2):1-26.
[12]Wiersma H, Nijstad N, Gautier T, et al, Scavenger receptor BI (SR-BI) facilitates hepatic very low density lipoprotein (VLDL) production in mice[J]. J. Lipid Res,2010 Mar:51(3):544-553.
[13]Calvo D,_Gomez-Coronado D, Lasuncion MA, et al, CLA-1 Is an 85-kD Plasma Membrane Glycoprotein That Acts as a High-Affinity Receptor for Both Native (HDL, LDL, and VLDL) and Modified (OxLDL and AcLDL) Lipoproteins[J]. Arterioscler Thromb Vasc Biol,1997.17(11):2341-2349.
[14]Gu X, K. Kozarsky, and M. Krieger, Scavenger Receptor Class B, Type I-mediated [3H]Cholesterol Efflux to High and Low Density Lipoproteins Is Dependent on Lipoprotein Binding to the Receptor[J]. J. Biol. Chem.,2000.275(39):29993-30001.
[15]Williams D.L, J.S. Wong, et al, SR-BI is required for microvillar channel formation and the localization of HDL particles to the surface of adrenocortical cells in vivo[J]. J. Lipid Res.,2002.43(4):544-549.
[16]Li X.-A, Titlow WB, Jackson BA, et al, High Density Lipoprotein Binding to Scavenger Receptor, Class B, Type I Activates Endothelial Nitric-oxide Synthase in a Ceramide-dependent Manner[J]. J. Biol. Chem.,2002.277(13):11058-11063.
[17]Miyazaki A, N.H., Horiuchi S, Scavenger receptors that recognize advanced glycation end products[J]. Trends Cardiovasc Med,2002 Aug.12(6):258-262.
[18]Li X.-A, Guo L, Dressman JL, et al, A Novel Ligand-independent Apoptotic Pathway Induced by Scavenger Receptor Class B, Type I and Suppressed by Endothelial Nitric-oxide Synthase and High Density Lipoprotein[J]. J. Biol. Chem.,2005.280(19):19087-19096.
[19]Barba G., Harper F, Harada T, et al, Hepatitis C virus core protein shows a cytoplasmic localization and associates to cellular lipid storage droplets[J]. Proceedings of the National Academy of Sciences of the United States of America,1997.94(4):1200-1205.
[20]Kawasaki Y., Nakagawa A, Nagaosa K, et al, Phosphatidylserine Binding of Class B Scavenger Receptor Type I, a Phagocytosis Receptor of Testicular Sertoli Cells[J]. Journal of Biological Chemistry,2002.277(30):27559-27566.
[21]Azhar S, A. Nomoto and E. Reaven, Hormonal regulation of adrenal microvillar channel formation[J]. J Lipid Res,2002.43:861-871.
[22]Acton, S, Scherer PE, Lodish HF, et al, Expression cloning of SR-BI, a CD36-related class B scavenger receptor[J]. J. Biol. Chem.,1994.269(33):21003-21009.
[23]Temel R, Trigatti B, DeMattos RB, et al, Scavenger receptor class B, type I (SR-BI) is the major route for the delivery of high density lipoprotein cholesterol to the steroidogenic pathway in cultured mouse adrenocortical cells[J]. Proc Natl Acad Sci USA,1997.94:13600-13605.
[24]Rigotti A T.B., Babitt J, et al. Scavenger receptor BI--a cell surface receptor for high density lipoprotein[J]. CUrrent Opinion in Lipidology,1997.8(3):181-188.
[25]Mardones P, Quinones V, Amigo L, et al, Hepatic cholesterol and bile acid metabolism and intestinal cholesterol absorption in scavenger receptor class B type I-deficient mice[J]. J. Lipid Res.,2001.42(2):170-180.
[26]Varban M.L., Rinninger Franz, Wang nang, et al, Targeted mutation reveals a central role for SR-BI in hepatic selective uptake of high density lipoprotein cholesterol[J]. Proceedings of the National Academy of Sciences of the United States of America,1998. 95(8):4619-4624.
[27]Kozarsky K.F, Donahee MH, Glick JM, et al, Gene Transfer and Hepatic Overexpres-sion of the HDL Receptor SR-BI Reduces Atherosclerosis in the Cholesterol-Fed LDL Receptor-Deficient Mouse[J]. Arterioscler Thromb Vasc Biol,2000.20(3):721-727.
[28]Wang N, Arai T. Ji Y, et al, Liver-specific Overexpression of Scavenger Receptor BI Decreases Levels of Very Low Density Lipoprotein ApoB, Low Density Lipoprotein ApoB, and High Density Lipoprotein in Transgenic Mice[J]. J. Biol. Chem.,1998. 273(49):32920-32926.
[29]Ueda Y, Royer L, Gong E, et al, Lower Plasma Levels and Accelerated Clearance of High Density Lipoprotein (HDL) and Non-HDL Cholesterol in Scavenger Receptor Class B Type I Transgenic Mice[J]. J. Biol. Chem.,1999.274(11):7165-7171.
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