糖基化终产物AGES对U937巨噬细胞高密度脂蛋白受体SRBI蛋白表达的影响.pdf
第15卷第8期 中国现代医学杂志 !Vol. 15 No. 8 2005年4月!China Journal of Modern Medicine!Apr. 2005 文章编号:1005- 8982(2005)08- 1136- 05 · 论著 · Effect?A B(c21C(-,?2?AB印迹法检测5R- 67蛋白的表达* 结果诱导分化后3934 细胞5R- 67表达在24+48 =逐渐升高)42 =下降,100+200和400 CD8E A012刺激后细胞表面5R- 67蛋白表 达量分别是65A组的1F44+2F38和2F44 倍 ; G0F05) ,400 CD8E的A012作用6+12+24+48 = 后) 3934巨噬细 胞5R- 67蛋白表达量分别为0 =的1F38+2F49+3F46和4F25 倍 HG0F05) * 结论诱导分化24及48 = 5R- 67 蛋白表达逐渐增加)而分化42 =蛋白表达下降,A012可增加3934巨噬细胞5R- 67蛋白表达且呈浓度和时间 依赖性* 关键词:糖基化终产物,巨噬细胞,高密度脂蛋白受体)清道夫受体 67,动脉粥样硬化 中图分类号:R363 文献标识码:A R?I?JK?L LM?N O?IF 02P 2004 1136·· There is a growing recognition that the risk of oc- currence for cardiovascular disease (CVD) in patients with diabetes comes up to that of nondiabetic patients and so does the worse prognosis1,2, which may be cor- related with some metabolic states of diabetes melli- tus. However, the pathogenesis of diabetes-associated CVD has not completely clarified. Among these, ad- vanced glycation end products (AGEs) have currently been believed to play a causative role in diabetic vas- culopathy including atherosclerosis(AS)as well as microangiopathy.AS is derived from ePcessive lipid deposition in the artery wall. Scavenger receptor class Q type R (SS-QR), which has been found recently and identified as a high density lipoprotein (HDT) recep- tor, mediates bi-directional fluP of cholesterol across the plasma membrane and plays an important role in eliminating the ePcrescent lipid from the cell in artery wall and the circulation. So it has been considered as an anti-atherogenic factorU. SS-QR has other ligands besides HDT, such as oP-TDT, ac-TDT, AGEs and so on. Rn the present study, we observe the influence of AGEs on the ePpression of SS-QR protein in VWUX macrophages and ePplore the change of SS-QR ePpres- sion in diabetic vasculopathy. ! “#$%? ?=( .5 $ABC ,632,(.5 5 89:; + 02 E+$ F/C ;? :.Ael0tiBe CA2D eEFression co7F0red Git: 9 :. HI7e0ns st0tistic0l di44erence is si6ni4ic0nt bJ Ct5dent t test HKL9.93MM. Figure 3 Effe t of 400 mg/L AGEs with different times on SR-BI protein expression in CDEF mGHrophGges E IisHussion ANOs/ lon6Pter7 Frod5cts o4 t:e Q0ill0rd re0ction d5e to :JFer6lJce7i0/ :0Be been s:oGn to 7od5l0te 0 B0rietJ o4 cell 45nctions/incl5din6 incre0sed B0sc5l0r Fer7e0bilitJ in t:e e0rlJ st06e o4 0t:ero6enesis/eE! Fression o4 0d:esion 7olec5les in t:e endot:eli0l cells le0din6 to t:e ind5ction o4 e0rlJ tr0nsendot:eli0l 7i! 6r0tion o4 7onocJtes 0nd sti75l0ted t:e rele0se o4 cJ! toRines s5c: 0s STUP! 0nd DVP1;le0din6 to t:e 0t:erosclerotic lesions Git: in4l0770torJ resFonses. Wn t:e ot:er :0nd; ANOs 70J Fro7ote t:ro7bosis 0nd t:e deBeloF7ent o4 0t:erosclerosis bJ ind5cin6 t:e in! cre0sedtiss5e40ctoreEFressiono47onocJteX 70croF:06es 0nd endot:eli0l cellsY3; 0nd ? :o5rs;G:ile on = :o5rs 04ter di44erenti0tion CAPD eEFression decre0sed to t:e leBel o4 t:0t be4ore di44erenti0tion. ir0no et 0lYZ. re! Forted t:0t eEFression o4 CAPD is loG in 4res:lJ iso! l0ted :570n 7onocJtes b5t incre0sed 5Fon n0t5r0l di44erenti0tion o4 t:ese cells. oGeBer; Q5r0o et 0lY19Z; 4o5ndin6 t:0t eEFression o4 CAPD in SKP1 cells; 0not:er :570n 7onocJtic le5Re7i0 cell line;de! cre0sed 4olloGin6 di44erence Git: KQA.We c0nnot cle0rlJ eEFl0in t:e di44erence.i44erent conditions o4 c5lt5rin6t:ecells0nddi44erentso5rceso4 70croF:06es 70J le0d to di44erent e44ects on t:e 0cti! B0tion o4 70croF:06es 0nd 70J res5lt in s5c: 0 dis! creF0ncJ.Dn t:e 4olloGin6 test;Ge 5se 70croF:06es di44erenti0tin6 ? : 0ccordin6 to t:e res5lt 0boBe. _a 70croF:06es t:0t Gere inc5b0ted in 7edi57 cont0inin6 ANOs s:oGed 0n incre0se in t:e leBels o4 CAPD;not onlJ 7ATA b5t 0lso Frotein;bot: in 0 ti7e 0nd dose deFendent 70nner.Dt :0s been s:oGn t:0t CAPD belon6s to one o4 7e7bers o4 ba * * * * 0 200 400 600 0%6%&2%24%4% !“#$%&“()*+,-(“./!“00&123 第8期彭扬,等:糖基化终产物AGEs对U937巨噬细胞高密度脂蛋白受体(SR_ BI) 蛋白表达的影响 113#% 1 LI LJ, Ma YM, NI LX, et al. 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(Edited by LONG Bai) (Continuation of the article on page 1135) there is another possibility. Like other members of the scavenger receptor family,SR-BI also binds to other native and modified lipoproteins,such as LDL,oEi! diFed LDL,and GGEs,Hhich may lead to the accu! mulation of cholesteryl esters Hithin cells of the arte! rial Hall. In summary,the eEpression levels of SR-BI in IJKL macrophages stimulated by GGEs is higher than that of non-stimulated IJKL cellsMGGEs stimulate SR-BI eEpression in a dose and time dependent man! ner, Hhich may be correlated Hith foam cell formation. NDL has a high affinity Hith SR-BI comparing Hith other SR-BI ligands.Ourther studies are necessary to eEplore Hhether high concentration of GGEs can com! pete Hith NDL, therefore, impair the cholesterol effluE of NDL. PQR LIN GS, TNEN TU, Li SV, et al. Insulin level analysis of the ratio of non-insulin-dependent diabetes mellitus occurring in coronary heart disease patientsPWR. Shongguo Uiandai XiEue SaFhi, YZZ, Q QY QK_-QKJ. Thinese PYR NIGNG SX,SNONG RN, Liang U, et al. Relationgship betHeen lipoproteina and activity of coagulation in old diabetic mellitusPWR. Shongguo Uiandai XiEue SaFhi, YZZ, QQL K-Ka. PKR WI X, WIGN B, bang N, et al. Scavenger receptor BIpromotes high density lipoprotein-mediated cellular cholesterol effluE PWR.W Biol Them, QJJL, YLYK YZJ_Y-YZJ_c. PR ONGGIN, NGGGI R, IdEOeO , et al. TDKa, a member of the class B scavenger receptor family, as a receptor for advanced glyca! tion end productsPWR. W Biol Them, YZZQ, YLac KQJc-KYZY. PcR STNIDe G, NORI O, TNEN WU, et al. Gdvanced glycation end! products interacting Hith their endothelial receptor induce eEpres! sion of vascular cell adhesion molecule-QfTG-Qin cultured human endothelial cells and in mice. G potential mechanism for the accelerated vasculopathy of diabetesPWR. W Tlin Invest, QJJc, JaK QKJc-QZK. PaR BIERNGIS G, ILLER e, dGSgER , et al. Gdvanced glycation end productGGE-mediated induction of tissue factor in cultured endothelial cells is dependent on RGGEPWR. Tirculation, QJJL, Ja L YYaY-YYLQ. PLR gLGee N and GORDON S. Is the class G macrophage scavenger re! ceptor SR-G multifunctionalh - ehe mousei s tale PWR. W Tlin In! vest, YZZQ, QZ_(c aJ-ac. P_R ONGGI N, NGGGI R, IdEOeO , et al. TDKa, a member of the class B scavenger receptor family, as a receptor for advanced glyca! tion end productsPWR. W Biol Them, YZZQ, YLa(c KQJc-KYZY. PJR NIRGNO d, XGGSNIeG S, NGdGGGbG X, et al. EEpression of human scavenger receptor class B typeIin cultured human mono! cyte-derived macrophages and atherosclerotic lesionsPWR. Tirc Res, QJJJ, _c(Q QZ_-QQa. PQZR IRGO d, eERgSeRG f, GREEN SR, et al. TharacteriFation of TLG-Q, a human homologue of rodent scavenger receptor BI, as a receptor for high density lipoprotein and apoptotic thymocytesPWR. W Biol Them, QJJL, YLY(Y_ QLccQ-QLccL. PQQR IbGSNIG X, EeO , NGeGG, et al. Gdvanced glycation end products-induced gene eEpression of scavenger receptors in cul! tured human monocyte-derived macrophages PWR.Biochem Biophys Res Tommun, YZZZ, YLL(Y Ka_-K_Z. (Edited by LONG Bai Referen es: 中国现代医学杂志 第15卷 ! 1140$
