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Multiple endocytic pathways of C protein-coupled receptors delineated by GIT1 sensitivity

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第3期97卷 1119-1124页

作者： Claing, A Perry, SJ Achiriloaie, M Walker, JKL Albanesi, JP Lefkowitz, RJ Premont, RT Duke Univ Med Ctr Howard Hughes Med Inst Durham NC 27710 USA Duke Univ Med Ctr Dept Med Durham NC 27710 USA Duke Univ Med Ctr Dept Biochem Durham NC 27710 USA Duke Univ Med Ctr Dept Cell Biol Durham NC 27710 USA Univ Texas SW Med Ctr Dept Pharmacol Dallas TX 75235 USA

Recently, we identified a GTPase-activating protein for the ADP ribosylation factor family of small GTP-binding proteins that we call GIT1, This protein initially was identified as an interacting partner for the G protein-coupled receptor kinases, and its overexpression was found to affect signaling and internalization of the prototypical beta(2)-adrenergic receptor. Here, we report that GIT1 overexpression regulates internalization of numerous, but not all, G protein-coupled receptors. The specificity of the GIT1 effect is not related to the type of C protein to which a receptor couples, but rather to the endocytic route it uses. GIT1 only affects the function of G protein-coupled receptors that are internalized through the clathrin-coated pit pathway in a beta-arrestin- and dynamin-sensitive manner. Furthermore, the GIT1 effect is not limited to G protein-coupled receptors because overexpression of this protein also affects internalization of the epidermal growth factor receptor. However, constitutive agonist-independent internalization is not regulated by GIT1, because transferrin uptake is not affected by GIT1 overexpression. Thus, GIT1 is a protein involved in regulating the function of signaling receptors internalized through the clathrin pathway and can be used as a diagnostic tool for defining the endocytic: pathway of a receptor.

关键词：衔接蛋白质类信号转导 COS细胞细胞周期蛋白质类细胞培养的黑长尾猴环AMP/生理学胞吞作用/生理学 GTP结合蛋白质类/生理学 GTP酶激活蛋白质类/生理学磷蛋白类受体血管紧张素 1型受体血管紧张素 2型受体内皮素B 受体肾上腺素能β/生理学受体血管紧张素/生理学受体细胞表面/生理学受体内皮缩血管肽/生理学受体毒蕈碱/生理学受体阿片样 μ/生理学受体血管活性肠肽/生理学重组融合蛋白质类/生理学转染动物人类

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Endogenous endothelin-1 depresses left ventricular systolic and diastolic performance in congestive heart failure

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期288卷 1214-1222页

作者： Onishi, K Ohno, M Little, WC Cheng, CP Wake Forest Univ Sch Med Cardiol Sect Winston Salem NC 27157 USA

Endothelin-1 (ET-1) is a positive inotrope in normal hearts;however, the direct cardiac effects of endogenous ET-1 in congestive heart failure (CHF) are unknown, We evaluated the cardiac responses to endogenous ET-1 using an ET, and ET, receptor blocker (L-754,142) in seven conscious dogs before and after pacing-induced CHF. Before CHF, when the plasma ET-1 was 7.3 +/- 1.7 fmol/ml, L-754,142 caused no significant alterations in heart rate, left Ventricular (LV) end-systolic pressure, total systemic resistance, and the time constant of LV relaxation (tau). LV contractile performance, measured by the slopes of LV pressure (P)-volume M relation (E-ES), dP/dt(max)-end-diastolic V relation (dE/dt(max)), and stroke work-end-diastolic V relation, was also unaffected. After CHF, when the plasma ET-1 was significantly increased to 14.1 +/- 3.0 fmol/ml (p < .05), L-754,142 produced a significant decreases in LV end-systolic pressure (101 +/- 11 versus 93 +/- 8 mm Hg) and total systemic resistance (0.084 +/- 0.022 versus 0.065 +/- 0.15 mm Hg/ml/min). The tau (42 +/- 12 versus 38 +/- 10 ms), mean left atrial P (22 +/- 5 Versus 18 +/- 4 mm Hg) (p < .05), and minimum LVP were also significantly decreased. After CHF, the slopes of P-V relations, E-ES (3.4 +/- 0.4 versus 4.8 +/- 0.8 mm Hg/ml), dE/dt(max) (42.4 +/- 7.8 versus 50.0 +/- 7.8 mm Hg/s/ml), and stroke work-end-diastolic V relation (58.1 +/- 3.3 versus 72.4 +/- 5.2 mm Hg) (p < .05) all increased after L-754,142, indicating enhanced contractility. Before CHF, low levels of endogenous ET-1 have little cardiac effect. However, after CHF, elevated endogenous ET-1 produces arterial vasoconstriction, slows LV relaxation, and depresses LV contractile performance. Thus, elevated endogenous ET-1 may contribute to the functional impairment in CHF in this canine model.

关键词：内皮缩血管肽1/血液内皮缩血管肽1/药理学内皮缩血管肽1/生理学硝普钠受体内皮缩血管肽/药物作用受体内皮缩血管肽/生理学时间因素心室功能障碍左/并发症动物狗

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Cytochrome P450 ω/ω-1 hydroxylase-derived eicosanoids contribute to endothelin_A and endothelin_B receptor-mediated vasoconstriction to endothelin-1 in the rat preglomerular arteriole

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期292卷 1153-1160页

作者： Hercule, HC Oyekan, AO New York Med Coll Dept Pharmacol Valhalla NY 10595 USA

The preglomerular arteriole of the rat was used to evaluate the contribution of cytochrome P450-derived eicosanoids to the vasoconstrictor effect of endothelin (ET)-1 and to determine the receptors mediating the response. ET-1 (4 X 10(-11) to 2 X 10(-9) M) produced dose-dependent reductions in the intraluminal diameter of the renal arteriole ranging from 25 +/- 8 to 142 +/- 16 mm. BMS182874 [(5-dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalenesulfonamide;3 mu M], an ETA receptor antagonist, or BQ788 (N-cis-2,6-dimethyl-piperidino-carbonyl-L-gamma-methylleucyl-D-1-methoxycarbonyl-tryptophanyl-D-norleucine;1 mu M), an ETB receptor antagonist, attenuated ET-1 vasoconstriction by 59 +/- 4 and 50 +/- 10%, respectively. The combined administration of both ET receptor antagonists increased inhibition of ET-1 vasoconstriction to 75 +/- 4%. 17-Octadecynoic acid (17-ODYA, 2 mM) or 12,12-dibromododecenoic acid (2 mM), inhibitors of 20-hydroxyeicosatetraenoic acid (20-HETE) production, attenuated ET-1-induced vasoconstriction by 50 +/- 6 and 40 +/- 3%, respectively, as did indomethacin (10 mM), an inhibitor of cyclooxygenase. Miconazole (2 mM), the epoxygenase inhibitor, was without effect. 20-HETE (10(-8) and 2 X 10(-8) M) elicited a dose-related vasoconstriction that was inhibited by 10 mu M, but not 5 mu M, indomethacin. The inhibition by 17-ODYA of ET-1 vasoconstriction was not greater when combined with BMS182874 or BQ788. Moreover, vasoconstriction induced by ET-3, an ETB-selective agonist, was inhibited by 17-ODYA. These data indicate that both ETA and ETB receptors mediate ET-1 vasoconstriction and that 20-HETE production linked to both receptors makes a major contribution to ET-1-induced renal arteriolar vasoconstriction in the rat.

关键词： 5 8 11 14-花生四烯酸/药理学烷烃1-单氧酶花生四烯酸/代谢小动脉/药物作用小动脉/生理学细胞色素P450酶系统/生理学丹磺酰化合物/药理学内皮缩血管肽1/药理学羟基花生四烯酸类/生理学肾/血液供给混合功能氧化酶类/生理学寡肽类/药理学哌啶类/药理学前列腺素内过氧化物合酶类/生理学大鼠 Sprague-Dawley 受体内皮素A 受体内皮素B 受体内皮缩血管肽/生理学血管收缩/药物作用动物男(雄)性大鼠

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Endothelin_B receptors are functionally important in mediating vasoconstriction in the systemic circulation in patients with left ventricular systolic dysfunction

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第4期33卷 932-938页

作者： Cowburn, PJ Cleland, JGF McArthur, JD MacLean, MR McMurray, JJV Dargie, HJ Morton, JJ Univ Glasgow MRC Clin Res Initiat Heart Failure Dept Cardiol Glasgow Lanark Scotland Univ Glasgow Western Infirm Glasgow G11 6NT Lanark Scotland Dept Cardiol Acad Unit Kingston Upon Hull Yorks England

OBJECTIVES This study was designed to assess the functional importance of endothelin (ET)(B) receptors in patients with left ventricular systolic dysfunction (LVSD) by comparing the hemodynamic effects of ET-1, a nonselective ETA and ETB agonist, with ET-3, a selective ETB receptor agonist. BACKGROUND Knowledge of the functional importance of ETB receptors in mediating vasoconstriction in chronic heart failure will help determine whether antagonists at both ETA and ETB receptors are required to fully prevent vasoconstriction to endogenously produced ET-1. METHODS We infused ET-1 (5 and 15 pmol/min) and ET-3 (5 and 15 pmol/min) into two separate groups of eight patients with LVSD with similar baseline hemodynamic indices. Hemodynamics were measured using a pulmonary thermodilution catheter and an arterial line. RESULTS Endothelin-l infusion led to systemic vasoconstriction, with a rise in mean arterial pressure (mean +/- SEM 100 +/- 3 to 105 +/- 3 mm Hg, p < 0.02) and systemic vascular resistance (1,727 +/- 142 to 2,055 +/- 164 dys/cm(-5), p < 0.001) and a fall in cardiac index (2.44 +/- 0.21 to 2.22 +/- 0.20 liters/min/m p < 0.01). Endothelin-3 infusion also led to systemic vasoconstriction, with a rise in mean arterial pressure (99 +/- 6 to 105 +/- 6 mm Hg, p < 0.01) and systemic vascular resistance (1,639 +/- 210 to 1,918 +/- 245 dyn/s/cm(-5), p < 0.01) and a fall in cardiac index (2.66 +/- 0.28 to 2.42 +/- 0.24 liters/min/m(2), p < 0.05). Pulmonary hemodynamic measurements did not change significantly in either group. CONCLUSIONS Both ET-1 and ET-3 infusions led to systemic vasoconstriction;the hemodynamic changes observed were of a similar magnitude at the same molar concentration. This suggests that ETB receptors are functionally important in mediating vasoconstriction, at least in the systemic circulation, in patients with LVSD. (J Am Coil Cardiol 1999;33:932-8) (C) 1999 by the American College of Cardiology.

关键词：慢性病内皮缩血管肽1/生理学内皮缩血管肽3/生理学血流动力学/生理学受体内皮素B 受体内皮缩血管肽/生理学心缩期/生理学血管收缩/生理学心室功能障碍左/病理生理学心室功能左/生理学老年人女(雌)性人类男(雄)性中年人

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Endothelin receptor pathway in human left ventricular myocytes: Relation to contractility

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ANNALS OF THORACIC SURGERY 2000年第3期69卷 711-715页

作者： Goldberg, AT Bond, BR Mukherjee, R New, RB Zellner, JL Crawford, FA Spinale, FG Med Univ S Carolina Div Cardiothorac Surg Charleston SC 29403 USA

Background. Increased synthesis and release of the potent bioactive peptide endothelin-l (ET-1) occurs during and after cardiac surgery. However, the cellular and molecular basis for the effects of ET-1 on human left ventricular (LV) myocyte contractility remains unknown. Methods. LV myocyte contractility was examined from myocardial biopsies taken from patients (n = 30) undergoing elective coronary artery bypass. LV myocytes (n = 997, > 30/patient) were isolated using microtrituration and contractility examined by videomicroscopy at baseline and after ET-1 exposure (200 pmol/L). In additional studies, myocytes were pretreated to inhibit either protein kinase C (PKC) (chelerythrine, 1 mu mol/L), the sodium/hydrogen (Na/H) exchanger (EIPA, 1 mu mol/L), both PKC and the Na/H exchanger, or the ETA receptor (BQ-123, 1 mu mol/L), followed with ET-1 exposure. Results. Basal myocyte shortening increased 37.8 +/- 6.3% with ET-1 (p < 0.05). Na/H exchanger, PKC, and dual inhibition all eliminated the effects of ET-1. Furthermore, ETA inhibition demonstrated that ET-1 effects on myocyte contractility were mediated through the ETA receptor subtype. Conclusions. ET-1 directly influences human LV myocyte contractility, which is mediated through the ETA receptor and requires intracellular activation of PKC and stimulation of the Na/H exchanger. (C) 2000 by The Society of Thoracic Surgeons.

关键词：细胞培养的心室/细胞学心肌收缩/生理学蛋白激酶C/拮抗剂和抑制剂受体内皮缩血管肽/生理学钠氢反向转运物/拮抗剂和抑制剂人类中年人

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Typical endothelin ET_A receptors mediate atypical endothelin-1-induced contractions in sheep isolated tracheal smooth muscle

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期289卷 1385-1390页

作者： Henry, PJ King, SH Univ Western Australia Dept Pharmacol Nedlands WA 6907 Australia

Contraction of vascular and nonvascular smooth muscle induced by the endothelin/sarafotoxin family of peptides frequently does not readily fit into the current classification criteria for ETA and ETB receptors, raising the possibility of additional atypical receptors. In the current study, isometric tension recording and radioligand binding techniques were used to characterize the ETA receptor population in sheep isolated tracheal smooth muscle. Endothelin-1 and sarafotoxin S6b induced similar concentration-dependent contractions, although endothelin-1 was 2.6-fold more potent (P < .05, n = 15-18), The ETA receptor-selective antagonists BQ-123 and FR139317 caused concentration-dependent inhibition of the contractions induced by endothelin-l and sarafotoxin S6b, but both antagonists were significantly less potent in inhibiting contractions induced by endothelin-l than sarafotoxin S6b. For example, 0.03 mu M FR139317 shifted the endothelin-1 and sarafotoxin S6b concentration-effect curves to the right by 1.8- and 8.3-fold, respectively (P < .01, n = 6-8). Although the observed agonist dependence of antagonist potency may indicate the presence of atypical ETA receptors, competition binding studies using I-125-endotheljn-1 and (125)-I-sarafotoxin S6b identified only a single population of BQ-123- and sarafotoxin S6b-sensitive ETA receptors, Additional association-, dissociation-, and saturation-binding studies revealed that I-125-endothelin-1 binding to these ETA receptors was pseudoirreversible, whereas I-125-sarafotoxin S6b binding was readily reversible. Thus, marked differences in the kinetic profiles of ETA receptor binding to endothelin-1, sarafotoxin S6b, and BQ-123, rather than the existence of another ETA receptor subtype, may explain the stark agonist dependence of antagonist potency observed in contractile studies.

关键词：吖庚因类/药理学结合竞争性内皮缩血管肽1/药理学吲哚类/药理学动力学肌收缩/药物作用肌收缩/生理学肌平滑/药物作用肌平滑/生理学肽类环/药理学放射配体测定受体内皮素A 受体内皮缩血管肽/拮抗剂和抑制剂受体内皮缩血管肽/代谢受体内皮缩血管肽/生理学绵羊气管/药物作用气管/生理学血管收缩药/药理学蝰蛇毒液类/药理学动物

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Regulation of guinea pig intestinal peristalsis by endogenous endothelin acting at ET_B receptors

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GASTROENTEROLOGY 2000年第1期119卷 80-88页

作者： Shahbazian, A Holzer, P Graz Univ Dept Expt & Clin Pharmacol A-8010 Graz Austria

Background & Aims: Endothelins are expressed in many enteric neurons of the gut. Because activation of endothelin ETA and ETB receptors is known to alter intestinal muscle activity, the effect of ETA and ETB receptor agonists and antagonists on propulsive peristalsis was examined, Methods: Repetitive peristalsis in fluid-perfused segments of the guinea pig isolated small intestine was elicited by a rise of the intraluminal pressure and recorded via the pressure changes generated by the peristaltic waves. Results: Endothelin 1 (0.3-10 nmol/L added to the organ bath) stimulated peristalsis as shown by a decrease in the pressure threshold at which peristaltic waves were triggered, whereas the endothelin analog sarafotoxin 6c (0.3-10 nmol/L) inhibited peristalsis as reflected by an increase in the pressure threshold. The ETA receptor antagonist BQ-123 (3 mu mol/L) converted the properistaltic action of endothelin 1 to an antiperistaltic action, whereas the ETB receptor antagonist BQ-788 (3 mu mol/L) prevented the antiperistaltic action of sarafotoxin 6c. BQ-788, but not BQ-123, facilitated peristalsis on its own, Additional experiments indicated that the properistaltic action of endothelin 1 is mediated by enteric neurons, whereas the peristaltic motor effects of sarafotoxin 6c and BQ-788 are caused by a direct action on the muscle. Conclusions: ETA receptor activation stimulates, whereas ETB, receptor activation inhibits, intestinal peristalsis. The ability of BQ-788 to facilitate peristalsis per se points to a physiologic role of ETB receptors in peristaltic motor regulation.

关键词：内皮缩血管肽类/生理学胃肠活动/生理学肠/神经支配肌平滑/药物作用神经元/生理学寡肽类/药理学肽类环/药理学哌啶类/药理学受体内皮素A 受体内皮素B 受体内皮缩血管肽/激动剂受体内皮缩血管肽/生理学蝰蛇毒液类/药理学动物豚鼠

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Enhanced endothelin_A receptor-mediated calcium mobilization and contraction in organ cultured porcine coronary arteries

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期295卷 484-491页

作者： Hill, BJF Katwa, LC Wamhoff, BR Sturek, M Univ Missouri Sch Med Dept Physiol Columbia MO 65212 USA Univ Missouri Dalton Cardiovasc Res Ctr Vasc Biol Lab Columbia MO 65212 USA E Carolina Univ Sch Med Dept Physiol Greenville NC USA

Arterial injury models for coronary artery disease have demonstrated an enhanced expression and function of either the endothelin(A) or endothelin(B) (ETA or ETB) receptor subtype. We hypothesized that organ culture would enhance the physiological function of ET receptors in the porcine right coronary artery. Arteries were either cold stored (4 degreesC) or organ cultured (37 degreesC) for 4 days. After 4 days, the artery was either 1) sectioned into rings to measure the ET-1-induced isometric tension response (3 x 10(-10)-3 x 10(-7) M), or 2) enzymatically dispersed and the isolated smooth muscle cells imaged using fura-2 to measure the myoplasmic calcium (Ca-m) response to 3 x 10(-8) M ET-1 (similar to EC50). Isometric tension and Ca-m to ET-1 were measured in the absence and presence of bosentan (nonselective ETA or ETB receptor antagonist), BQ788 (ETB-selective antagonist), and BQ123 (ETA-selective antagonist). Compared with cold storage, organ culture induced a 2-fold increase in tension development (3 x 10(-7) M ET-1) and Ca-m (3 x 10(-8) M ET-1), which was inhibited with bosentan, thus confirming the enhanced responses to ET-1 were due to ET receptor activation. BQ123 also inhibited the enhanced contraction and Ca-m responses to ET-1. In contrast, BQ788 failed to inhibit tension development and Ca-m responses to ET-1 in organ culture and cold storage. Sarafotoxin 6C (ETB agonist) failed to elicit an increased Ca-m response in organ culture compared with cold storage. Our results indicate the increased tension development and Ca-m responses to ET-1 in organ culture are attributable to ETA receptors, and not ETB receptors.

关键词：抗高血压药/药理学钙/代谢冠状血管/药物作用冠状血管/生理学低温保存内皮缩血管肽1/药理学等长收缩/药物作用等长收缩/生理学动力学肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/生理学寡肽类/药理学器官培养技术肽类环/药理学哌啶类/药理学受体内皮素A 受体内皮素B 受体内皮缩血管肽/激动剂受体内皮缩血管肽/拮抗剂和抑制剂受体内皮缩血管肽/生理学磺胺类/药理学猪血管收缩药/药理学蝰蛇毒液类/药理学动物

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An endothelin receptor antagonist ameliorates injuries of sinusoid lining cells in porcine liver transplantation (vol 178, pg 64, 1999)

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AMERICAN JOURNAL OF SURGERY 1999年第5期178卷 436-436页

作者： Fukanaga, K Takada, Y Mei, G Taniguchi, H Seino, K Yuzawa, K Otsuka, M Todoroki, T Goto, K Fukao, K Department of Surgery Institute of Clinical Medicine University of Tsukuba Tsukuba City Ibaraki Japan

Background: TAK-044 is an endothelin receptor antagonist. Whether the agent has protective effects on liver graft injuries from non–heart-beating donors is ***: In donor pigs, cardiac arrest was induced by stopping the respirator. Forty-five minutes after cessation of the respirator, the liver was flushed with University of Wisconsin (UW) solution, preserved for 8 hours at 4°C, and transplanted orthotopically. The pigs were divided into two groups: a control group and a drug-treated group in which TAK-044 was given in the UW solutions (10 mg/L) and was administered to recipients (10 mg/kg body weight).Results: TAK-044 treatment significantly increased recipient survival rate. After reperfusion of the graft, portal venous pressure and 15-minute retention rate of indocyanine green were significantly reduced in the drug-treated group. Electron microscopic findings indicated that TAK-044 attenuated endothelial cell ***: TAK-044 treatment improves the viability of livers harvested from non–heart-beating donors. The main effect of the agent is protection of endothelial cells from ischemia/reperfusion injuries.

关键词：移植物存活心脏停搏肝移植/方法肽类环受体内皮缩血管肽/拮抗剂和抑制剂受体内皮缩血管肽/生理学再灌注损伤/预防和控制猪组织供者动物

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Mechanisms of endothelin-induced venoconstriction in isolated guinea pig mesentery

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第2期289卷 762-767页

作者： Johnson, RJ Fink, GD Galligan, JJ Michigan State Univ Dept Pharmacol & Toxicol E Lansing MI 48824 USA

In the present study, endothelin (ET) agonists and receptor selective antagonists were used to characterize ET receptors mediating constriction in guinea pig mesenteric veins (250-300 mu m diameter) in vitro. The contribution of ET-evoked vasodilator release to venous tone was also explored. Computer-assisted video microscopy was used to monitor vein diameter. Endothelin-1 (ET-1), endothelin-3 (ET-3), and sarafotoxin 6c (S6c) produced sustained concentration-dependent contractions with a rank order agonist potency of ET-1 = S6c > ET-3. Indomethacin (1 mu M) and Na-nitro-L-arginine (100 mu M) enhanced ET-1 and S6c responses. The ETA selective antagonists BQ-610 (100 nM) and PD156707 (10 nM) shifted ET-1 concentration-response curves rightward and decreased maximal ET-1 responses, without changing S6c responses. The ETB selective antagonist BQ-788 (100 nM) shifted S6c responses rightward but produced no change in ET-1 responses. Combined application of BQ-788 and BQ-610 or BQ-788 and PD 156707 produced a rightward shift in ET-1 responses that was greater than shifts produced by BQ-610 or PD 156707 alone. In conclusion, smooth muscle in guinea pig mesenteric veins expresses ETA and ETB receptors coupled to contractile mechanisms. Activation of endothelial ETB receptors results in release of vasodilators, primarily nitric oxide.

关键词：环加氧酶抑制药/药理学内皮缩血管肽1/药理学内皮缩血管肽2/药理学内皮缩血管肽3/药理学酶抑制剂/药理学吲哚美辛/药理学显微镜检查电视肌张力/药物作用肌平滑血管/药物作用一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢硝基精氨酸/药理学受体内皮缩血管肽/拮抗剂和抑制剂受体内皮缩血管肽/生理学内脏循环/药物作用血管收缩/药物作用血管收缩药/药理学静脉蝰蛇毒液类/药理学动物豚鼠男(雄)性

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