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Role of polyamine structure in inhibition of K⁺-Cl^- cotransport in human red cell ghosts

JOURNAL OF PHYSIOLOGY-LONDON 1999年第3期520卷 723-735页

作者： Sachs, JR Martin, DW SUNY Stony Brook Dept Med Stony Brook NY 11794 USA

1. K(+)-Cl(-) cotransport in human red cell ghosts is inhibited by divalent inorganic cations, soluble polycations and amphipathic organic cations. These findings suggest a common mechanism of inhibition, namely, binding of the cations to negative charges at the surface of a hydrophobic structure. 2. We have characterized the inhibitory capacity of a number of polyamines in order to obtain information about the nature of the charges with which they interact. Neomycin inhibited swelling-stimulated cotransport. The diquaternary amines dimethonium and decamethonium were relatively ineffective inhibitors. These compounds are thought to shield negative charges, but not bind to them. 3. Comparison of a homologous series of polyamines indicated that primary amines were better inhibitors than secondary amines, that inhibition increased with the charge of the polyamine, and that inhibition increased as the distance separating the amines increased. 4. The results indicate that the negative charges to which polycations bind are multiple and mobile. Since they must be associated with a hydrophobic environment, it is likely that they are negatively charged phospholipids located in the inner leaflet of the bilayer membrane. 5. Heating red cells or ghosts to 49 degrees C denatures spectrin. Heating markedly increased K(+) uptake in swollen ghosts but not in shrunken ghosts. The increase in uptake was reversed when swollen ghosts were shrunk even though denaturation of spectrin was not reversed. Polyamines, which inhibited swelling-activated K(+) uptake in control ghosts, similarly inhibited the increased uptake in heated ghosts. 6. We speculate that spectrin, which is closely associated with the inner bilayer leaflet, shields negative charges in a volume-dependent manner and so regulates volume-sensitive K(+) transport.

关键词：胺类/化学胺类/药理学载体蛋白质类/拮抗剂和抑制剂载体蛋白质类/血液红细胞膜/代谢红细胞/细胞学红细胞/代谢新霉素/药理学聚胺类/化学聚胺类/代谢聚胺类/药理学溶解度协同转运子人类

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Low cerebrospinal fluid hypocretin (orexin) and altered energy homeostasis in human narcolepsy

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ANNALS OF NEUROLOGY 2001年第3期50卷 381-388页

作者： Nishino, S Ripley, B Overeem, S Nevsimalova, S Lammers, GJ Vankova, J Okun, M Rogers, W Brooks, S Mignot, E Stanford Univ Ctr Narcolepsy Palo Alto CA 94304 USA Leiden Univ Med Ctr Dept Neurol & Clin Neurophysiol Leiden Netherlands Charles Univ Fac Med 1 Dept Neurol Prague Czech Republic

Hypocretins (orexins) are hypothalamic neuropeptides involved in sleep and energy homeostasis. Hypocretin mutations produce narcolepsy in animal models. In humans, narcolepsy is rarely due to hypocretin mutations, but this system is deficient in the cerebrospinal fluid (CSF) and brain of a small number of patients. A recent study also indicates increased body mass index (BMI) in narcolepsy. The sensitivity of low CSF hypocretin was examined in 38 successive narcolepsy-cataplexy cases [36 human leukocyte antigen (HLA)-DQB1*0602-positive] and 34 matched controls (15 controls and 19 neurological patients). BMI and CSF leptin levels were also measured. Hypocretin-1 was measurable (169 to 376pg/ml) in all controls. Levels were unaffected by freezing/thawing or prolonged storage and did not display any concentration gradient. Hypocretin-1 was dramatically decreased (< 100pg/ml) in 32 of 38 patients (all HILA-positive). Four patients had normal levels (2 HLA-negative). Two HLA-positive patients had high levels (609 and 637pg/ml). CSF leptin and adjusted BMI were significantly higher in patients versus controls. We conclude that the hypocretin ligand is deficient in most cases of human narcolepsy, providing possible diagnostic applications. Increased BMI and leptin indicate altered energy homeostasis. Sleep and energy metabolism are likely to be functionally connected through the hypocretin system.

关键词：方差分析人体质量指数载体蛋白质类/血液载体蛋白质类/脑脊髓液能量代谢/生理学 HLA-DQ抗原/脑脊髓液内环境稳定细胞内信号肽和蛋白质类瘦素/脑脊髓液发作性睡病/脑脊髓液发作性睡病/诊断神经肽类/血液神经肽类/脑脊髓液青少年成年人老年人女(雌)性人类男(雄)性中年人

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Tropomyosin isoform 5b is expressed in human erythrocytes: implications of tropomodulin-TM5 or tropomodulin-TM5b complexes in the protofilament and hexagonal organization of membrane skeletons

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BLOOD 2000年第4期95卷 1473-1480页

作者： Sung, LA Gao, KM Yee, LJ Temm-Grove, CJ Helfman, DM Lin, JJC Mehrpouryan, M Univ Calif San Diego Dept Bioengn La Jolla CA 92093 USA Univ Calif San Diego Ctr Genet Mol La Jolla CA 92093 USA Univ Arizona Dept Nutr Sci Tucson AZ 85721 USA Cold Spring Harbor Lab Cold Spring Harbor NY 11724 USA Univ Iowa Dept Biol Sci Iowa City IA 52242 USA

The human erythrocyte membrane skeleton consists of hexagonal lattices with junctional complexes containing F-actin protofilaments of approximately 33-37 nm in length. We hypothesize that complexes formed by tropomodulin, a globular capping protein at the pointed end of actin filaments, and tropomyosin (TM), a rod-like molecule of approximately 33-35 nm, may contribute to the formation of protofilaments, We have previously cloned the human tropomodulin complementary DNA and identified human TM isoform 5 (hTM5), a product of the gamma-TM gene, as one of the major TM isoforms in erythrocytes, We now identify TM5b, a product of the alpha-TM gene, to-be the second major TM isoform, TM5a, the alternatively spliced isoform of the (U-TM gene, which differs by 1 exon and has a weaker actin-binding affinity, however, is not present. TM4, encoded by the delta-TM gene, is not present either. In sodium dodecyl sulfate-polyacrylamide gel electrophoresis, hTM5 comigrated with the slower TM major species in erythrocyte membranes, and hTM5b comigrated with the faster TM major species. TM5b, like TM5, binds strongly to tropomodulin, more so than other TM isoforms, The 2 major TM isoforms, therefore, share several common features: They have 248 residues, are approximately 33-35 nm long, and have high affinities toward F-actin and tropomodulin. These common features may be the key to the mechanism by which protofilaments are formed. Tropomodulin-TM5 or tropomodulin-TM5b complexes may stabilize F-actin in segments of approximately 33-37 nm during erythroid terminal differentiation and may, therefore, function as a molecular ruler. TM5 and TM5b further define the hexagonal geometry of the skeletal network and allow actin-regulatory functions of TMs to be modulated by tropomodulin, (C) 2000 by The American Society of Hematology.

关键词：氨基酸序列载体蛋白质类/血液载体蛋白质类/化学克隆分子细胞骨架/超微结构红细胞膜/超微结构红细胞/代谢红系祖细胞/代谢红系祖细胞/超微结构微丝蛋白质类/血液微丝蛋白质类/化学分子序列数据蛋白质亚型/血液蛋白质亚型/化学蛋白质亚型/遗传学重组蛋白质类/化学重组蛋白质类/代谢序列比对序列同源性氨基酸原肌球调节蛋白质原肌球蛋白/血液原肌球蛋白/化学原肌球蛋白/遗传学动物人类大鼠

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Role of heart-type fatty acid-binding protein in early detection of acute myocardial infarction

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CLINICAL CHEMISTRY 2000年第5期46卷 718-719页

作者： Ghani, F Wu, AHB Graff, L Petry, C Armstrong, G Prigent, F Brown, M Hartford Hosp Dept Pathol & Lab Med Ishikari Hokkaido 06102 Japan New Britain Gen Hosp New Britain CT 06050 USA Bayer Diagnost Tarrytown NY 10591 USA Winthrop Univ Hosp Mineola NY 11501 USA

Biochemical evidence of acute myocardial infarction (AMI) is delayed by the delay of appearance of serum cardiac markers in the blood after myocardial injury. Heart-type fatty acid-binding protein (H-FABP), a small (15 kDa) cytoplasmic protein (1) involved in lipid homeostasis, is abundant in heart muscle (2). H-FABP is ~10-fold lower in skeletal muscle than in heart muscle, and the amounts in the kidney, liver, and small intestine are even lower (3). After myocardial damage, H-FABP is released into the intercellular space and appears in the bloodstream (4). The magnitude of the increase in plasma H-FABP has also demonstrated a good correlation with the size of the infarction (5). Myoglobin, another small protein (18 kDa), appears in the plasma within 2–3 h after myocardial infarction and is considered a useful marker in the early detection of AMI (6). Myoglobin lacks specificity because myoglobin released from skeletal muscles cannot be distinguished from that released from the heart. Cardiac troponin I (cTnI) and creatine kinase MB isoenzyme (CK-MB) are more specific for myocardial injury but lack early sensitivity because their blood concentrations do not increase appreciably until 6–8 h after the onset of AMI (7).

关键词：载体蛋白质类/血液载体蛋白质类/代谢胸痛/血液胸痛/诊断肌酸激酶/血液脂肪酸结合蛋白质类脂肪酸类/代谢同工酶类髓磷脂P2蛋白质/血液髓磷脂P2蛋白质/代谢心肌梗死/血液心肌梗死/诊断心肌/代谢肌红蛋白/血液肿瘤蛋白质类肌钙蛋白I/血液肿瘤抑制蛋白质类女(雌)性人类男(雄)性中年人

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Mannose binding lectin (MBL) genotype distributions with relation to serum levels in UK Caucasoids

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EUROPEAN JOURNAL OF IMMUNOGENETICS 2000年第3期27卷 111-117页

作者： Crosdale, DJ Ollier, WER Thomson, W Dyer, PA Jensenious, J Johnson, RWG Poulton, KV Univ Manchester Sch Epidemiol & Hlth Sci Manchester M13 9PT Lancs England Manchester Royal Infirm Transplantat Lab Manchester M13 9WL Lancs England Univ Aarhus Dept Med Microbiol Aarhus Denmark Manchester Royal Infirm Renal Transplant Unit Manchester M13 9WL Lancs England

Mannose binding lectin (MBL) gene and promoter-region polymorphisms contribute to a reduction in the levels of circulating MBL in a number of ways. Promoter polymorphisms affect the levels of MBL produced, whilst structurally encoding mutations cause non-functional protein to be assembled and subsequently degraded. MBL is important as a protein of the innate immune system in both the clearance of potential pathogens and the activation of the complement cascade. Using variations of SSP-PCR amplifications and SSO probing techniques, we have produced MEL-polymorphism haplotype and genotype profiles of a series of high-level MEL-producing, low-level MEL-producing and random individuals taken from a population of 800 UK Caucasoid controls. Structurally encoding mutant alleles were more frequent within the low-level producing cohort when compared to both high-level producers and the randomly selected sample. However, not all low-level producers could be accounted for by the possession of low-level encoding haplotypes. This may be due to the presence of additional, undetected polymorphisms governing MBL production, or another external factor that may influence the transcriptional regulation of the gene.

关键词：等位基因载体蛋白质类/血液载体蛋白质类/遗传学胶凝素类欧洲大陆世系人群/遗传学基因频率/遗传学基因型大不列颠/流行病学单元型/遗传学寡核苷酸探针/遗传学点突变/遗传学多态现象遗传/遗传学启动区(遗传学)/遗传学人类

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The association of variant mannose-binding lectin genotypes with radiographic outcome in rheumatoid arthritis

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ARTHRITIS AND RHEUMATISM 2000年第3期43卷 515-521页

作者： Graudal, NA Madsen, HO Tarp, U Svejgaard, A Jurik, AG Graudal, HK Garred, P Aarhus Univ Hosp DK-8000 Aarhus Denmark Natl Univ Hosp Copenhagen Denmark

Objective. To investigate the possible association of mannose-binding lectin (MBL) genotypes with the outcome of rheumatoid arthritis (RA), Methods. MBL genotypes and plasma concentrations were retrospectively determined in 140 RA patients who were selected from a major cohort followed up prospectively for up to 32 years. Results, MEL-insufficient patients (those with 2 defective structural MBL alleles or with 1 defective allele combined with a low-expression variant of the normal allele) had unfavorable outcomes. The relative risk of a severe radiographic outcome event (30% of maximum radiographic destruction, or an RE30) was 3.1 (95% confidence interval 1.8-5.1) in the MBL-insufficient group versus the MEL-competent group (P < 0.0001). An RE30 occurred in 50% of MBL-competent patients within 17 years, while such an event occurred 9 years earlier in MBL-insufficient patients (i.e., within 8 years) (P < 0.0001), During the first 15 years, there was a significant trend toward lower hemoglobin levels (P < 0.04), higher erythrocyte sedimentation rates (P < 0.02), and a higher number of swollen joints (P < 0.05) in the MEL-insufficient group. Conclusion, MBL genotypes giving rise to MBL insufficiency are highly significant risk factors for fast progression of radiographic joint destruction.

关键词：等位基因关节炎类风湿/遗传学关节炎类风湿/放射摄影术载体蛋白质类/血液载体蛋白质类/遗传学胶凝素类基因型杂合子回顾性研究治疗结果变异(遗传学) 青少年成年人女(雌)性人类男(雄)性中年人

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Regulation of Na⁺-K⁺-2C1^- cotransport by protein phosphorylation in ferret erythrocytes

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第3期517卷 699-708页

作者： Flatman, PW Creanor, J Univ Edinburgh Sch Med Dept Biomed Sci Physiol Membrane Biol Grp Edinburgh EH8 9AG Midlothian Scotland

1. Na+-K+-2Cl(-) cotransport in ferret erythrocytes was measured as the bumetanide-sensitive uptake of Rb-86. 2. The resting cotransport rate was high but could be increased threefold by treating erythrocytes with calyculin A, a potent inhibitor of serine/threonine phosphatases. Twenty nanomolar was sufficient to maximally and rapidly (within 4 min) stimulate transport. 3. The effects of sever al kinase inhibitors were tested. High concentrations of K-252a, K-252b, calphostin C and hypericin caused less than 20% inhibition. Staurosporine (IC50, 0.06 mu M) and 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP1;IC50, 2.5 mu M) were more potent but still only partially (40-50%) inhibited transport, an effect mimicked by reducing ionized intracellular Mg2+ concentration to submicromolar levels. Genistein may inhibit all transport at a sufficiently high dose (IC50, 0.36 mM) perhaps by directly inhibiting the transporter. 4. Staurosporine, PP1 and the removal of Mg2+ all prevented subsequent stimulation by calyculin A and all inhibited calyculin-stimulated transport by 20-30%. The effects of staurosporine, PP1 and Mg2+ removal were not additive. 5. The phosphatase that dephosphorylates the cotransporter is probably Mg2+ (or possibly Ca2+ or Mn2+) sensitive and not the tar get for calyculin A. The data suggest that this phosphatase is inhibited by phosphorylation, and that it is the regulation of this process which is affected by calyculin A and the kinase inhibitors tested here. Phosphorylation of the phosphatase is probably regulated by members of the Src family of tyrosine kinases.

关键词：血蛋白质类/代谢载体蛋白质类/血液氯化物/血液酶抑制剂/药理学红细胞/药物作用红细胞/代谢雪貂内环境稳定动力学镁/血液模型生物学恶唑类/药理学磷酰化钾/血液吡唑类/药理学嘧啶类/药理学铷/血液钠/血液钠钾氯化物协同转运子星状孢子素/药理学动物

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Concentrations of lipopolysaccharide-binding protein, bactericidal/permeability-increasing protein, soluble CD14 and plasma lipids in relation to endotoxaemia in patients with alcoholic liver disease

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ALCOHOL AND ALCOHOLISM 2002年第1期37卷 81-86页

作者： Schäfer, C Parlesak, A Schütt, C Bode, JC Bode, C Robert Bosch Krankenhaus Dept Internal Med Div Gastroenterol D-70376 Stuttgart Germany Univ Hohenheim Dept Physiol Nutr D-70599 Stuttgart Germany Ernst Moritz Arndt Univ Greifswald Dept Immunol D-17489 Greifswald Germany

There is increasing evidence that gut leakage in persons with chronic alcohol misuse leads to endotoxaemia, which might contribute to the development of alcoholic hepatitis or cirrhosis. In addition, it was recently shown that the endotoxin-binding capacity of whole blood is reduced in these patients. To analyse this phenomenon, we measured the concentration of functionally important endotoxin-binding plasma components which modify the action of endotoxin. In patients with minimal (n = 10), intermediate (n = 9), and cirrhotic alcoholic liver disease (n = 11), and healthy controls (n = 11), plasma endotoxin was determined in a limulus assay. The concentration of lipoproteins was assessed by measuring apolipoproteins, the other factors were directly measured in immunoassays. In the entire group of alcoholics, endotoxin and the concentration of binding factors that are involved in the action of endotoxin on its target cells (LPS-binding protein and sCD14) were increased. Endotoxin antagonists, such as bactericidal/permeability-increasing protein and high-density lipoprotein, were increased in the pre-cirrhotic stages, whereas a significant reduction of the latter was observed in cirrhosis. Low-density lipoprotein remained unchanged. The elevation of binding factors in the pre-cirrhotic stages of alcoholic liver disease might attenuate the effects of endotoxaemia, whereas in cirrhosis the reduction of high density lipoprotein, to which large quantities of endotoxin bind, may contribute to its pro-inflammatory effects.

关键词：急相蛋白质类慢性酒精中毒/血液慢性酒精中毒/病因学抗微生物阳离子肽类血蛋白质类/分析载体蛋白质类/血液色谱法内毒素血症/血液内毒素血症/并发症酶联免疫吸附测定免疫测定脂类/血液肝疾病酒精性/血液肝疾病酒精性/并发症膜糖蛋白类膜蛋白质类成年人女(雌)性人类男(雄)性中年人

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MULTIVALENT LIGAND-BINDING BY SERUM MANNOSE-BINDING PROTEIN

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ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 1992年第1期299卷 129-136页

作者： LEE, RT ICHIKAWA, Y KAWASAKI, T DRICKAMER, K LEE, YC JOHNS HOPKINS UNIV MCCOLLUM PRATT INSTBALTIMOREMD 21218 KYOTO UNIV FAC PHARMACEUT SCIDEPT BIOL CHEMKYOTO 606JAPAN COLUMBIA UNIV DEPT BIOCHEM & MOLEC BIOPHYSNEW YORKNY 10032

The serum-type mannose-binding protein (MBP) is a defense molecule that has carbohydrate-dependent bactericidal effects. It shares with mammalian and chicken hepatic lectins similarity in the primary structure of the carbohydrate-recognition domain, as well as the ligand-binding mode: a high affinity (KD approximately nM) is generated by clustering of approximately 30 terminal target sugar residues on a macromolecule, such as bovine serum albumin, although the individual monosaccharides have low affinity (KD 0.1-1 mM). On the other hand, MBP does not manifest any significant affinity enhancement toward small, di- and trivalent ligands, in contrast to the hepatic lectins whose affinity toward divalent ligands of comparable structures increased from 100- to 1000-fold. Such differences may be explained on the basis of different subunit organization between the hepatic lectins and MBP.

关键词：急相蛋白质类/代谢碳水化合物序列载体蛋白质类/血液细胞膜/代谢糖肽类/化学合成糖肽类/药理学糖蛋白类/代谢糖苷类/药理学动力学配体甘露糖/代谢甘露糖结合凝集素类分子序列数据单糖类/药理学酵母菌酿酒/代谢动物大鼠

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GROWTH-HORMONE AND INSULIN-LIKE GROWTH-FACTOR REGULATE INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN-1 IN LARON TYPE DWARFISM, GROWTH-HORMONE DEFICIENCY AND CONSTITUTIONAL SHORT STATURE

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ACTA ENDOCRINOLOGICA 1992年第4期127卷 351-358页

作者： LARON, Z SUIKKARI, AM KLINGER, B SILBERGELD, A PERTZELAN, A SEPPALA, M KOIVISTO, VA HELSINKI UNIV CENT HOSPDEPT MED 2HAARTMANINKATU 4SF-00290 HELSINKIFINLAND UNIV HELSINKI HOSP CENTDEPT OBSTET & GYNECOL 1SF-00100 HELSINKI 10FINLAND TEL AVIV UNIV SACKLER FAC MEDBEILINSON MED CTRIL-69978 TEL AVIVISRAEL

Insulin-like growth factors (IGFs) mediate the effects of growth hormone (GH), and the insulin-like growth factor-binding proteins (IGFBPs) modulate the actions of IGFs in tissues. We studied the circulating levels of IGFBP-1 in 6 children and 9 adults with Laron type dwarfism (LTD), in 11 children and 21 adults with growth hormone deficiency (GHD), and in 8 children with constitutional short stature. Compared with the situation in healthy children, the basal serum IGFBP-1 concentration was 5.4-fold higher in LTD children. 4.1-fold higher in GHD children, and 3.8-fold higher in children with short stature (p < 0.02 vs controls in all groups). in adult patients with multiple pituitary hormone deficiency (MPHD), the IGFBP-1 concentration was 2-fold elevated, but it was normal in adult LTD patients. Intravenous (N = 10) or subcutaneous (N = 9) administration of IGF-I (75 ***-1 and 150 ***-1, respectively) in LTD children resulted in a rapid 50-60% fall in serum insulin (p < 0.02), a decline in blood glucose and a concomitant 40-60% rise of IGFBP-1 levels (p < 0.05). Treatment for seven days with IGF-I (150 ***-1.d-1) resulted in a decrease by 34% and 44% of serum IGFBP-1 level in two out of three children with LTD. After prolonged GH therapy, the IGFBP-1 level fell in GHD children by 29% (p < 0.05), in GHD adults by 52% (p < 0.02) and in children with constitutional short stature by 1 7% (p < 0.02). IGFBP-1 and insulin concentrations were inversely related in patients with GHD (r= -0.66, p < 0.001) or with LTD (r = -0.57, p < 0.05). Our data suggest that: (a) increased IGFBP-1 concentration in LTD, GHD and constitutional short children may, at least in part, be accounted for by an IGF-I deficiency, (b) both the rise in IGF-I and a fall in insulin contributed to the rise in IGFBP-1 after acute IGF-I administration;(c) prolonged IGF-I or GH treatment causes a persistent decline in IGFBP-1 concentration. In conclusion, IGF-I and GH may regulate IGFBP-1 secretion

关键词：身高/药物作用载体蛋白质类/血液侏儒症/药物疗法侏儒症/代谢侏儒症/病理学生长激素/血液生长激素/缺乏生长激素/治疗应用注射静脉内胰岛素/血液胰岛素样生长因子结合蛋白质1 胰岛素样生长因子Ⅰ/分析胰岛素样生长因子Ⅰ/治疗应用生长调节素类/分析成年人儿童女(雌)性人类男(雄)性

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