Hyperglycemia promotes overexpression of SR-BII isoform of the scavenger receptor class B type I in type 2 diabetes mellitus: A study in Juana Koslay City, San Luis, Argentina

The scavenger receptor class B type I (SR-BI) is a high-density lipoprotein (HDL) receptor involved in reverse cholesterol transport. Some studies reported the association to be stronger in the presence of diabetes. The full length gene encoding SR-BI is comprised in 13 exons that are alternatively spliced to produce two major transcripts: the full length SR-BI and the splice variant SR-BII, in which exon 12 is skipped. Considering that type 2 diabetes status is characterized by changes in the concentration of plasma lipids, modifications in lipoprotein size and composition, which may be important modulators of the SR-BI expression;the aims of the study were to examine the influence of SR-BI polymorphism (rs838895) on lipid profile and SR-BI mRNA expression in a population of diabetic patients living in Juana Koslay City. Blood samples were drawn from controls (n = 40) and Type 2 diabetic patients (n = 66) and DNA and total RNA were obtained. SR-BI mRNA expression was measured by RT-PCR and SR-BI polymorphism was detected by Tetra Primer ARMSPCR. Compared to controls, diabetic patients had higher fasting serum glucose, glycated hemoglobin, triglycerides, total cholesterol, lowdensity lipoprotein cholesterol, and lower highdensity lipoprotein cholesterol. SR-BI mRNA expression was lower in T2DM when compared to controls, suggesting that the hyperglycemia presents in T2DM patients down-regulates SR-BI mRNA expression. Interestingly, we found that decreased SR-BI expression resulted in markedly increased plasma LDL concentrations in T2DM subjects, and the overexpression of SRBII isoform is responsible for the markedly increased plasma LDL-c concentrations. The polymorphism (rs838895) did not modify the mRNA level of SR-BI in leucocytes from control and diabetic patients. This study provides novel evidence suggesting that hyperglycemia may affect reverse cholesterol transport by controlling SRBI expression in diabetic patients. LDL cholesterol levels are associated with low SR-BI mRNA expression in T2DM.

Expression pattern and tissue localization of the class B scavenger receptor BmSCRBQ4 in Bombyx moil

Class B scavenger receptors （SR-Bs） are cell surface glycoproteins involved in various physiological processes in vivo, including the transport and metabolism of lipids, binding and phagoeytosis of xenobiotics, and signaling. But little information is available about silkworm SR-Bs; it is necessary to study these SR-Bs for revealing their function. In this study, we cloned the full-length coding sequence of BrnSCRBQ4, a SR-B gene from the silkworm Bombyx mori L. We found that the BmSCRBQ4 gene consists of nine exons and eight introns, with an open reading frame of 1371 bp encoding 456 amino acids. Gene expression studies determined that BmSCRBQ4 messenger RNA （mRNA） was expressed in unfertilized eggs, during embryonic development and throughout the majority of the larval period. Expression of mRNA was detected in the mid gut, middle silk gland, posterior silk gland, head, integumentum, fat body, testes and the ovaries of the larval B. mori Dazao strain, as well as in the silkworm cell lines BmN and BmE. Protein expression studies found BmSCRBQ4 protein was expressed only in the testes, fat body and middle silk gland of larvae, as well as in the silkworm cell lines BmN and BmE. The BmSCRBQ4 protein showed variability in banding patterns in different tissues and cells when analyzed by Western blotting. Immunohistochemical staining showed that the BmSCRBQ4 protein localizes to the constitutive membranes or cellular membranes of these tissues. These results indicated that BmSCRBQ4 gene may play some physiologically relevant roles at the cell surface in each tissue.

Scavenger Receptor Class B type 1(SR-B1)and the modifiable risk factors of stroke

Stroke is a devastating disease that occurs when a blood vessel in the brain is either blocked or ruptured,consequently leading to deficits in neurological function.Stroke consistently ranked as one of the top causes of mortality,and with the mean age of incidence decreasing,there is renewed interest to seek novel therapeutic treatments.The Scavenger Receptor Class B type 1(SR-B1)is a multifunctional protein found on the surface of a variety of cells.Research has found that that SR-B1 primarily functions in an anti-inflammatory and antiatherosclerotic capacity.In this review,we discuss the characteristics of SR-B1 and focus on its potential correlation with the modifiable risk factors of stroke.SR-B1 likely has an impact on stroke through its interaction with smoking,diabetes mellitus,diet,physical inactivity,obesity,hypercholesterolemia,atherosclerosis,coronary heart disease,hypertension,and sickle cell disease,all of which are critical risk factors in the pathogenesis of stroke.

Effect of Shengqing capsule on serum cholesterol content and hepatic scavenger receptor class B of rats with cholesterol calculus

Objective To observe the effect of Shengqing Capsule(SC)on serum contents of TC,LDL-C,and HDLC,hepatic scavenger receptor BⅠ(SRBⅠ),and CD36 in rats with cholesterol calculus.Methods

虹鳟Scarb1基因克隆、生物信息学及组织表达分析

清道夫受体B类成员1(scavenger receptor class B member 1,Scarb1)作为细胞表面的膜受体蛋白,在动物体色形成过程中发挥重要作用。为了解Scarb1基因在虹鳟(Oncorhynchus mykiss)体色形成中的作用,通过RACE技术克隆虹鳟Scarb1基因的cDNA全长,并运用生物信息学方法分析该基因及其序列结构特征,同时使用实时定量PCR(qRT-PCR)检测Scarb1基因在虹鳟、金鳟及其杂交F_(1)代不同发育阶段和不同组织中的表达情况。结果显示,Scarb1基因cDNA序列全长为2032 bp,开放阅读框1479 bp,编码492个氨基酸,预测分子质量为55.59 ku,且存在保守的CD36结构域和2个跨膜区。序列同源性分析显示,虹鳟与其他硬骨鱼类的氨基酸序列相似度为71.69%~98.58%;进化分析发现虹鳟与大马哈鱼亲缘关系最近,与哺乳动物和两栖动物亲缘关系最远。qRT-PCR检测结果表明,在虹鳟与金鳟胚胎期及出膜后各发育阶段中Scarb1基因均有不同程度表达,且表现为受精期至桑葚期的表达显著高于其他时期(P<0.05),对虹鳟与金鳟同一时期的差异分析发现该基因在胚胎期及7 dph(days post hatch)、1 M(month post hatch)、2 M和3 M时期中表达存在显著差异(P<0.01)。Scarb1基因在虹鳟与金鳟背部皮肤和背部肌肉等色素沉着性组织中表达量较高,其中在金鳟背部皮肤的表达量显著高于虹鳟(P<0.01)。此外,Scarb1基因在杂交F_(1)代不同发育时期中的表达规律与双亲一致;在不同组织中,该基因在杂交F_(1)代背部皮肤中的表达量介于双亲之间。研究结果表明,Scarb1基因与虹鳟体色形成有着密切关系,且可能在金鳟黄色体色形成过程中发挥重要作用。

B类1型清道夫受体介导的高密度脂蛋白在年龄相关性黄斑变性中的研究进展

随着年龄的增长,机体胆固醇代谢失调和叶黄素水平异常易导致视网膜异常脂质沉积和玻璃膜疣,进而增加年龄相关性黄斑变性(age-related macular degeneration,AMD)的患病风险。视网膜细胞上的B类1型清道夫受体(scavenger receptor class B type 1,SR-B1)在脂质代谢和视网膜保护中至关重要。组织细胞表面的SR-B1通过识别并结合细胞外的高密度脂蛋白(high-density lipoprotein,HDL),将游离胆固醇逆向转运至肝脏,对维持全身包括视网膜的脂质代谢平衡与避免脂质沉积至关重要。此外,HDL同样作为转运体参与叶黄素的视网膜转运过程。叶黄素,以其独特的蓝光过滤和抗氧化功能,减少蓝光对视网膜的潜在损伤并清除有害的氧自由基,发挥保护视网膜的作用。本综述将详细探讨SR-B1在视网膜中的作用,尤其是在协助胆固醇清除和叶黄素抗氧化防御方面的重要性,并评述SR-B1以及携带的有益成分如HDL和叶黄素对缓解AMD发病的机制与最新研究进展。

壳寡糖上调SRBI核心岩藻糖基化修饰水平减弱小鼠动脉粥样硬化斑块形成

目的 从蛋白糖基化修饰角度探讨壳寡糖(COS)减弱动脉粥样硬化(AS)斑块形成的机制。方法 将40只ApoE-/-小鼠随机分为对照组和COS组。对照组饲给予高脂饲料12周,COS组给予高脂饲料+COS(每天灌胃,500 mg/kg)12周。全自动生化分析仪检测两组小鼠的血脂水平并对主动脉斑块切片进行HE和油红O染色。凝集素芯片、液相色谱-串联质谱、酶联免疫吸附试验检测血清中糖蛋白变化。胆固醇酯流出实验和游离胆固醇酯测定实验评价清道夫受体B类成员1(SRBI)糖基化修饰位点改变对巨噬细胞胆固醇流出量的影响。结果 COS显著降低小鼠TC和LDL-C水平(P<0.05),但对TG、HDL-C、ApoA1和ApoB100无影响。与对照组相比,COS组主动脉内膜厚度和斑块大小明显变薄、变小(P<0.05)。两组小鼠血清中变化最明显的小扁豆凝集素(LCA)结合蛋白分子量为80~90 ku,清道夫受体B类成员1为其中之一。COS促进了细胞内胆固醇的流出,抑制了游离胆固醇酯的积累(P<0.05)。SRBI敲低或N108糖基化位点突变可抑制COS引起的胆固醇流出,增加细胞内游离胆固醇的积累(P<0.05)。结论 COS通过增加SRBI糖基化水平促进脂质外排,从而减少动脉粥样硬化的形成。

On the Impairment of Stress-Induced Changes in Triglyceride Levels via a Sub-Toxic Dose of Unmethylated Cytidine Phosphate Guanosine Oligodinucleotide (a Toll-Like Receptor 9 Ligand)

Changes in lipid metabolism have been implicated in protection against infectious diseases. In the first experiment of this study, we measured clinical lipid parameters in a murine model where the unmethylated cytidine phosphate guanosine (CpG) oligodinucleotide (ODN1826), a Toll-like receptor 9 (TLR9) agonist was administered in combination with D-galactosamine (GalN) that caused relatively liver-specific inflammation and toxicity. In the control mice group injected with phosphate-buffered saline (PBS) (acute psychological stress model associated with blood sampling), the serum triglyceride (TG) levels showed a rapid decrease followed by a rebound at 24 h as we have recently reported. However, such a TG rebound was impaired in the CpG/GalN- and solely CpG-treated groups of mice despite an absence of liver injury based on serum alanine aminotransferase levels in the latter group. Thus, the stress-associated serum TG rebound was abrogated by the injection of a sub-hepatotoxic CpG dose. In the second experiment, we simply measured the hepatic CD36 and SACRB1 (the gene for scavenger receptor B1 (SR-B1)) transcripts after the i.p. administration of PBS, CpG or CpG/GalN. There was a remarkable elevation of hepatic CD36 transcript expression in both the CpG- and CpG/GalN-treated mice at 8 h post-CpG injection whereas the increase in the PBS-treated mice was slower than the former two groups, suggesting that hepatic CD36 transcript expression is more pronounced in the combined stress models than under psychological stress alone. The individual mice data showed that the increase in CD36 expression was accompanied by a reduction in SCARB1 mRNA, showing reciprocal regulation between these two genes. Together with our previously reported findings, these data suggest that, in a murine model combining psychological stress with TLR-triggered hepatic inflammation, the psychological stress facilitates liver uptake of plasma TG (and its components fatty acids), but the subsequent re-esterification and/or release of TG-rich lipoproteins from the liver is impaired due to the concomitant TLR-signaling. We hypothesize that lipid metabolism during acute stress shifts toward an elevated hepatic uptake of lipids due to concomitant TLR signaling, facilitating the clearance of bacterial lipids by the liver.

Scavenger receptor BI: A multi-purpose player in cholesterol and steroid metabolism

Scavenger receptor class B type Ⅰ (SR-BI) is an important member of the scavenger receptor family of integral membrane glycoproteins. This review highlights studies in SR-BI knockout mice, which concern the role of SR-BI in cholesterol and steroid metabolism. SR-BI in hepatocytes is the sole molecule involved in selective uptake of cholesteryl esters from high-density lipoprotein (HDL). SR-BI plays a physiological role in binding and uptake of native apolipoprotein B (apoB)-containing lipoproteins by hepatocytes, which identif ies SR-BI as a multipurpose player in lipid uptake from the blood circulation into hepatocytes in mice. In adrenocortical cells, SR-BI mediates the selective uptake of HDL-cholesteryl esters, which is eff iciently coupled to the synthesis of glucocorticoids (i.e. corticosterone). SR-BI knockout mice suffer from adrenal glucocorticoid insuff iciency, which suggests that functional SR-BI protein is necessary for optimal adrenal steroidogenesis in mice. SR-BI in macrophages plays a dual role in cholesterol metabolism as it is able to take up cholesterol associated with HDL and apoBcontaining lipoproteins and can possibly facilitate cholesterol efflux to HDL. Absence of SR-BI is associated with thrombocytopenia and altered thrombosis susceptibility, which suggests a novel role for SR-BI in regulating platelet number and function in mice. Transgenic expression of cholesteryl ester transfer protein in humanized SR-BI knockout mice normalizes hepatic delivery of HDL-cholesteryl esters. However, other pathologies associated with SR-BI def iciency, i.e. increased atherosclerosis susceptibility, adrenal glucocorticoid insuffi ciency, and impaired platelet function are not normalized, which suggests an important role for SR-BI in cholesterol and steroid metabolism in man. In conclusion, generation of SR-BI knockout mice has signif icantly contributed to our knowledge of the physiological role of SR-BI. Studies using these mice have identif ied SR-BI as a multi-purpose player in cholesterol and steroid metabolism because it has distinct roles in reverse cholesterol transport, adrenal steroidogenesis, and platelet function.

清道夫受体B1基因启动子甲基化与冠心病的关联分析

目的 探讨清道夫受体B1(SCARB1)基因启动子区域甲基化与冠心病发病的关联性。方法 选取2018年12月至2020年5月在上海交通大学医学院附属仁济医院就诊的120例冠心病患者作为病例组,并随机选取同期健康体检人群中性别和年龄匹配的140名健康受试者作为对照组,进行病例对照研究。采用亚硫酸盐转化,扩增目标区域后采用高通量测序对基因组进行甲基化检测,分析两组SCARB1基因启动子区域CpG位点的甲基化差异。结果 病例组SCARB1+67基因的甲基化水平显著高于对照组(P<0.001),SCARB1+134基因的甲基化水平显著低于对照组(P<0.001),且在男性(P均<0.001)、女性(P均<0.001)冠心病患者中与对照组比较差异有统计学意义。病例组SCARB1基因的平均甲基化水平显著低于对照组[(80.27±2.14)%比(81.11±1.27)%;P=0.006],且只在男性冠心病患者中差异有统计学意义(P=0.002)。结论 SCARB1基因的甲基化水平与冠心病的发病存在关联,可能参与其发生发展过程。

Potential PET Ligands for Imaging of Cerebral VPAC and PAC Receptors: Are Non-Peptide Small Molecules Superior to Peptide Compounds?

Pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) have been known for decades to mediate neuroendocrine and vasodilative actions via G-protein-coupled receptors of Class B. These are targets of imaging probes for positron emission tomography (PET) or single photon emission tomography (SPECT) in tumor diagnostics and tumor grading. However, they play only a subordinate role in the development of tracers for brain imaging. Difficulties in development of non-peptide ligands typical for cerebral receptors of PACAP and VIP are shared by all members of Class B receptor family. Essential landmarks have been confirmed for understanding of structural details of Class B receptor molecular signalling during the last five years. High relevance in the explanation of problems in ligand development for these receptors is admitted to the large N-terminal?ectodomain markedly different from Class A receptor binding sites and poorly suitable as orthosteric binding sites for the most small-molecule compounds. The present study is focused on the recently available receptor ligands for PAC1, VPAC1 and VPAC2 receptors as well as potential small-molecule lead structures suitable for use in PET or SPECT. Recently, biaryl, cyanothiophene and pentanamide structures with affinities in nM-range have been proposed as non-peptide ligands at VPAC1 and VPAC2 receptors. However, most of these ligands have been classified as non-competitive related to the orthosteric binding site of endogenous peptide ligands of VPAC receptors. For PAC1 receptors have been identified hydrazide compounds for which an inhibitory and potentially competitive mechanism of receptor binding has been postulated based on molecular docking studies.

Genetic variants of the class A scavenger receptor gene are associated with coronary artery disease in Chinese

The class A scavenger receptor, encoded by the macrophage scavenger receptor 1 （MSR1） gene, is a pattern recognition receptor （PPR） primarily expressed in macrophages. It has been reported that genetic polymorphisms of MSR1 are significantly associated with the number of diseased vessels and coronary artery narrowing greater than 20% in Caucasians. However, whether it links genetically to coronary artery disease （CAD） in Chinese is not defined. Here, we performed an independent case-control study in a Chinese population consisting of 402 CAD cases and 400 controls by genotyping ten single nucleotide polymorphisms （SNPs） of MSR1. We found that rs416748 and rs13306541 were significantly associated with an increased risk of CAD with per allele odds ratio （OR） of 1.56 [95% confidence interval （CI） = 1.28-1.90; P 〈 0.001] and 1.70 （95% CI = 1.27-2.27; P 〈 0.001）, re- spectively. Our results indicate that genetic variants of MSR1 may serve as predictive markers for the risk of CAD / in combination with traditional risk factors of CAD in Chinese population.

下调清道夫受体B类成员1表达对胃癌细胞AGS增殖、迁移及侵袭的影响

目的探讨清道夫受体B类成员1(SCARB1)对胃癌细胞(AGS)增殖、迁移及侵袭的影响及其机制。方法采用RT-qPCR和Western blot检测SCARB1在人胃黏膜上皮细胞GES1和人胃癌细胞AGS中的表达水平;将AGS细胞随机分为空白对照组、阴性对照组和实验组,在实验组中使用RNA干扰技术下调SCARB1表达,阴性对照组使用siRNA阴性序列进行转染,空白对照组不转染siRNA;克隆形成实验和细胞计数试剂盒-8(CCK-8)法评估各组细胞增殖能力,流式细胞术检测各组细胞凋亡情况,细胞划痕实验和Transwell实验分析各组细胞横向迁移、纵向迁移和侵袭能力,Western blot检测基质金属蛋白酶2(MMP2)、基质金属蛋白酶9(MMP9)及PI3K/AKT通路相关蛋白的表达。结果与GES1细胞比较,SCARB1在AGS中表达升高(P<0.05),AGS细胞SCARB1干扰效率为(68.06±2.04)%;实验组细胞克隆形成率下降,在转染24 h、48 h及72 h时细胞活力均低于阴性对照组,实验组细胞凋亡率高于阴性对照组(P<0.05),阴性对照组与空白对照组比较,差异无统计学意义;实验组在24 h和48 h的平均划痕宽度大于阴性对照组,48 h时细胞迁移和侵袭数量少于阴性对照组(P<0.05),阴性对照组与空白对照组比较,差异无统计学意义;实验组MMP2、MMP9、AKT、p-AKT(ser473)、PI3K(p110)表达下降,p-AKT/AKT减少(P<0.05),阴性对照组与空白对照组比较,差异无统计学意义。结论SCARB1在AGS中高表达,下调SCARB1表达作用于PI3K/AKT信号通路和MMP2、MMP9蛋白而抑制胃癌细胞AGS增殖、迁移和侵袭,促进其凋亡。

Glucose-regulated protein 78 inhibits scavenger receptor A-mediated internalization of acetylated low density lipoprotein

Class A scavenger receptor(SR-A) plays an important role in foam cell formation.However, the mechanism underlying the internalization of the receptor-ligand complexes remains unclear.The aim of the present study was to investigate the molecular mechanism to regulate SR-A-mediated intracellular lipid accumulation in macrophages A pull-clown assay was performed and glucoseregulated protein 78(GRP78) was identified to bind with the cytoplasmic domain of SR-A(CSR-A).Immunoprecipitation and artificially expressed protein binding assay demonstrated the direct specific binding of GRP78 with SR-A in cells.Indirect immunofluorescence assay and western blot analysis showed their co-localization in membrane and cytoplasm.Over-expression of GRP78 specifically inhibited SR-A-mediated uptake of fluorescent acetylated low-density lipoprotein, a specific ligand for SR-A, without altering cellular SR-A expression and binding ability, and significantly inhibited cholesterol ester accumulation in cells, which can be partly attributed to the suppression of c-Jun-NH2-terminal kinase signaling pathway.These results suggest that GRP78 may act as an inhibitor of SR-A-mediated internalization of modified low-density lipoprotein into macrophages(C) 2009 Elsevier Inc.All rights reserved.

家蚕B型清道夫受体基因的鉴定及系统发生与表达分析

B型清道夫受体(SR-B)是清道夫受体超基因家族成员,参与机体的脂类代谢、动脉粥样硬化形成或保护、宿主免疫损害防御、凋亡细胞清除和细胞粘附等重要生命过程。基于家蚕全基因组数据,利用比较基因组学方法,鉴定获得了14个家蚕B型清道夫受体基因,这些基因分布在至少5条染色体上,其内含子的大小从几十到近万个碱基对。系统发生分析表明,14个家蚕B型清道夫受体基因分布在3个类群:第1类群中分布的9个基因和第3类群中分布的3个基因,分别与类群中其它昆虫的同源基因形成明显的直系同源关系;第2类群中分布有2个基因,此类群中不同昆虫的同源基因之间的进化关系较为复杂。EST数据和芯片数据分析表明,多数家蚕B型清道夫受体基因具有转录活性。RT-PCR检测结果显示,有8个家蚕B型清道夫受体基因在5龄第3天幼虫组织中表达,并具有不同的表达模式,推测这些基因可能行使不同的功能。研究结果为进一步诠释家蚕B型清道夫受体基因的功能奠定了基础。

高密度脂蛋白对THP-1巨噬细胞B类Ⅰ型清道夫受体的表达及胆固醇流出的影响

目的:观察高密度脂蛋白(HDL)对THP-1巨噬细胞B类Ⅰ型清道夫受体(SR-BI)的表达及胆固醇流出的影响。方法:用HDL及氧化低密度脂蛋白(ox-LDL)处理THP-1细胞,采用RT-PCR、Western印迹及液体闪烁计数法观察细胞SR-BI的表达及细胞内胆固醇流出的变化。结果:ox-LDL下调THP-1巨噬细胞中SR-BI的表达,而HDL则上调THP-1巨噬细胞中SR-BI的表达;液体闪烁计数法检测发现ox-LDL减少细胞中胆固醇的流出,HDL可以增加细胞胆固醇的流出,且HDL的效应呈浓度依赖性。结论:HDL可能通过上调THP-1巨噬细胞SR-BI的表达,促进巨噬细胞内胆固醇流出。

Biliary cholesterol secretion: More than a simple ABC

Biliary cholesterol secretion is a process important for 2 major disease complexes, atherosclerotic cardiovascular disease and cholesterol gallstone disease. With respect to cardiovascular disease, biliary cholesterol secretion is regarded as the f inal step for the elimination of cholesterol originating from cholesterol-laden macrophage foam cells in the vessel wall in a pathway named reverse cholesterol transport. On the other hand, cholesterol hypersecretion into the bile is considered the main pathophysiological determinant of cholesterol gallstone formation. This review summarizes current knowledge on the origins of cholesterol secreted into the bile as well as the relevant processes and transporters involved. Next to the established ATP-binding cassette (ABC) transporters mediating the biliary secretion of bile acids (ABCB11), phospholipids (ABCB4) and cholesterol (ABCG5/G8), special attention is given to emerging proteins that modulate or mediate biliary cholesterol secretion. In this regard, the potential impact of the phosphatidylserine flippase ATPase class Ⅰ type 8B member 1, the Niemann Pick C1-like protein 1 that mediatescholesterol absorption and the high density lipoprotein cholesterol uptake receptor, scavenger receptor class B type Ⅰ, is discussed.

马氏珠母贝B型清道夫受体PmSR-B基因克隆与表达性分析

采用c DNA末端快速扩增技术克隆获得马氏珠母贝清道夫受体基因c DNA全长序列(Pm SR-B);利用荧光定量技术检测Pm SR-B基因在各个组织中的表达量。结果表明,Pm SR-B基因c DNA序列全长1 857 bp,开放阅读框(ORF)长1 443 bp,编码480个氨基酸,5′非翻译区(5′UTR)长89 bp,3′UTR长325 bp。预测其分子质量为54.77 ku,等电点为7.94,脂溶性系数92.94,总平均亲水性-0.120,属于疏水性蛋白;不稳定指数26.37,属于稳定蛋白。氨基酸序列同源比对结果,Pm SR-B氨基酸序列与其他物种具有一定的保守性,与华贵类栉孔扇贝(Mimachlamys nobilis)SR-B的序列的相似度高达47%。荧光定量PCR检测结果,Pm SR-B在肝胰腺中表达量最高,其后依次是鳃、闭壳肌、中央膜,各组织的表达量差异具统计学意义(P<0.05)。

B类清道夫受体与胆囊结石关系的研究进展

B类清道夫受体作为机体内广泛分布的一类高密度胆固醇受体,主要参与调节脂质代谢、介导胆固醇和其他脂质体在高密度脂蛋白和细胞之间转换、促进胆固醇从外周组织流出,并促进肝脏对胆固醇的选择性摄取,通过肝内胆管将胆固醇分泌入胆汁。因此,作为参与调节脂质代谢的B类清道夫受体能够影响胆汁胆固醇的水平,而胆汁胆固醇过饱和作为胆囊胆固醇结石发生的必要条件,其所介导的胆固醇代谢在胆囊结石过程中扮演的角色已经逐步显现。

婴幼儿脑干脑炎EV71-VP1、PSGL-1和SCARB2的表达

目的观察人肠道病毒71型(enterovirus 71,EV71)、P选择素糖蛋白配体1(P-selectin glycoprotein ligand-1,PSGL-1)和人清道夫受体B2(scavenger receptor B2,SCARB2)在婴幼儿脑干脑炎的表达,探究PSGL-1、SCARB2与EV71间的联系及EV71感染人体后可能的侵染途径和机制。方法收集EV71-VP1染色阳性的10例婴幼儿的器官、组织进行PSGL-1、SCARB2免疫组织化学染色,并与EV71-VP1免疫组织化学染色结果相比较。结果 EV71-VP1在脑内神经元、胶质细胞、血管周呈"袖套样"浸润的炎症细胞,胃底腺壁细胞呈强阳性;肺泡巨噬细胞,肠腺上皮细胞及黏膜层淋巴小结、腭扁桃体中淋巴细胞呈中度阳性;肠系膜淋巴结、脾的淋巴细胞中呈弱阳性。PSGL-1仅在胃底腺壁细胞,腭扁桃体隐窝鳞状上皮组织,肺泡巨噬细胞及各组织白细胞中表达。SCARB2除肠、脾组织外均有表达。结论 SCARB2与EV71组织分布具有相关性,在病毒的侵染及复制过程中起重要作用。胃可能是EV71复制的一个重要部位。