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VASCULAR DYSFUNCTION IN THE Α-GALACTOSIDASE A-KNOCKOUT MOUSE IS AN ENDOTHELIAL CELL-, PLASMA MEMBRANE-BASED DEFECT
dc.contributor.authorPark, James L.en_US
dc.contributor.authorWhitesall, Steven E.en_US
dc.contributor.authorD’alecy, Louis G.en_US
dc.contributor.authorShu, Limingen_US
dc.contributor.authorShayman, James A.en_US
dc.date.accessioned2010-06-01T22:09:20Z
dc.date.available2010-06-01T22:09:20Z
dc.date.issued2008-10en_US
dc.identifier.citationPark, James L; Whitesall, Steven E; D’Alecy, Louis G; Shu, Liming; Shayman, James A (2008). "VASCULAR DYSFUNCTION IN THE Α-GALACTOSIDASE A-KNOCKOUT MOUSE IS AN ENDOTHELIAL CELL-, PLASMA MEMBRANE-BASED DEFECT." Clinical and Experimental Pharmacology and Physiology 35(10): 1156-1163. <http://hdl.handle.net/2027.42/75176>en_US
dc.identifier.issn0305-1870en_US
dc.identifier.issn1440-1681en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/75176
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=18565198&dopt=citationen_US
dc.format.extent477881 bytes
dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherBlackwell Publishing Asiaen_US
dc.rights© 2008 Blackwell Publishing Asia Pty Ltden_US
dc.subject.otherEndotheliumen_US
dc.subject.otherFabry Diseaseen_US
dc.subject.otherΑ-Galactosidase Aen_US
dc.subject.otherGlobotriaosylceramideen_US
dc.titleVASCULAR DYSFUNCTION IN THE Α-GALACTOSIDASE A-KNOCKOUT MOUSE IS AN ENDOTHELIAL CELL-, PLASMA MEMBRANE-BASED DEFECTen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelPharmacy and Pharmacologyen_US
dc.subject.hlbsecondlevelPhysiologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum* Division of Nephrology, Department of Internal Medicine, University of Michigan Medical Center,en_US
dc.contributor.affiliationumDepartment of Surgery, University of Michigan Medical School, Ann Arbor anden_US
dc.contributor.affiliationumDepartment of Surgery, William Beaumont Hospital, Royal Oak, Michigan, USAen_US
dc.contributor.affiliationotherDepartment of Molecular and Integrative Physiology,en_US
dc.identifier.pmid18565198en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/75176/1/j.1440-1681.2008.04984.x.pdf
dc.identifier.doi10.1111/j.1440-1681.2008.04984.xen_US
dc.identifier.sourceClinical and Experimental Pharmacology and Physiologyen_US
dc.identifier.citedreferenceKint JA. The enzyme defect in Fabry's disease. Nature 1970; 227: 1173.en_US
dc.identifier.citedreferenceKint JA. Fabry's disease: Alpha-galactosidase deficiency. Science 1970; 167: 1268 – 9.en_US
dc.identifier.citedreferenceSweeley CC, Klionsky B. Fabry's disease: Classification as a sphingolipidosis and partial characterization of a novel glycolipid. J. Biol. Chem. 1963; 238: 3148 – 50.en_US
dc.identifier.citedreferenceBrady RO, Gal AE, Bradley RM, Martensson E, Warshaw AL, Laster L. Enzymatic defect in Fabry's disease. Ceramidetrihexosidase deficiency. N. Engl. J. Med. 1967; 276: 1163 – 7.en_US
dc.identifier.citedreferenceDesnick RJ, Ioannou YA, Eng CM. Α-Galactosidase A deficiency: Fabry disease. In: Scriver CR, Beaudet AL, Sly WS, Valle D (eds). The Metabolic and Molecular Bases of Inherited Disease, 8th edn. McGraw-Hill, New York. 2001; 3733 – 74.en_US
dc.identifier.citedreferenceDesnick RJ, Banikazemi M, Wasserstein M. Enzyme replacement therapy for Fabry disease, an inherited nephropathy. Clin. Nephrol. 2002; 57: 1 – 8.en_US
dc.identifier.citedreferenceEitzman DT, Bodary PF, Shen Y et al. Fabry disease in mice is associated with age-dependent susceptibility to vascular thrombosis. J. Am. Soc. Nephrol. 2003; 14: 298 – 302.en_US
dc.identifier.citedreferenceShu L, Murphy HS, Cooling L, Shayman JA. An in vitro model of Fabry disease. J. Am. Soc. Nephrol. 2005; 16: 2636 – 45.en_US
dc.identifier.citedreferenceOhshima T, Murray GJ, Swaim WD et al. Alpha-Galactosidase A deficient mice: A model of Fabry disease. Proc. Natl Acad. Sci. USA 1997; 94: 2540 – 4.en_US
dc.identifier.citedreferenceShen Y, Bodary PF, Vargas FB et al. Alpha-galactosidase A deficiency leads to increased tissue fibrin deposition and thrombosis in mice homozygous for the factor V Leiden mutation. Stroke 2006; 37: 1106 – 8.en_US
dc.identifier.citedreferenceBodary PF, Shen Y, Vargas FB et al. Alpha-galactosidase A deficiency accelerates atherosclerosis in mice with apolipoprotein E deficiency. Circulation 2005; 111: 629 – 32.en_US
dc.identifier.citedreferenceMoore DF, Gelderman MP, Fuhrmann SR, Schiffmann R, Brady RO, Goldin E. Fabry disease and vascular risk factors: Future strategies for patient-based studies and the knockout murine model. Acta Paediatr. Suppl. 2006; 95: 69 – 71.en_US
dc.identifier.citedreferenceHeare T, Alp NJ, Priestman DA et al. Severe endothelial dysfunction in the aorta of a mouse model of Fabry disease: Partial prevention by N -butyldeoxynojirimycin treatment. J. Inherit. Metab. Dis. 2007; 30: 79 – 87.en_US
dc.identifier.citedreferenceWhitesall SE, Hoff JB, Vollmer AP, D’Alecy LG. Comparison of simultaneous measurement of mouse systolic arterial blood pressure by radiotelemetry and tail-cuff methods. Am. J. Physiol. Heart Circ. Physiol. 2004; 286: H2408 – 15.en_US
dc.identifier.citedreferenceTang EH, Ku DD, Tipoe GL, Feletou M, Man RY, Vanhoutte PM. Endothelium-dependent contractions occur in the aorta of wild-type and COX2 −/– knockout but not COX1 −/– knockout mice. J. Cardiovasc. Pharmacol. 2005; 46: 761 – 5.en_US
dc.identifier.citedreferenceFaraci FM, Sigmund CD, Shesely EG, Maeda N, Heistad DD. Responses of carotid artery in mice deficient in expression of the gene for endothelial NO synthase. Am. J. Physiol. 1998; 274: H564 – 70.en_US
dc.identifier.citedreferencePark JL, Loberg RD, Duquaine D et al. GLUT4 facilitative glucose transporter specifically and differentially contributes to agonist-induced vascular reactivity in mouse aorta. Arterioscler. Thromb. Vasc. Biol. 2005; 25: 1596 – 602.en_US
dc.identifier.citedreferenceTang EH, Feletou M, Huang Y, Man RY, Vanhoutte PM. Acetylcholine and sodium nitroprusside cause long-term inhibition of EDCF-mediated contractions. Am. J. Physiol. Heart Circ. Physiol. 2005; 289: H2434 – 40.en_US
dc.identifier.citedreferenceZhou Y, Varadharaj S, Zhao X, Parinandi N, Flavahan NA, Zweier JL. Acetylcholine causes endothelium-dependent contraction of mouse arteries. Am. J. Physiol. Heart Circ. Physiol. 2005; 289: H1027 – 32.en_US
dc.identifier.citedreferenceShayman JA, Killen PD. Fabry disease. In: Mount DB, Pollak MJ (eds). Molecular and Genetic Basis of Renal Disease. Saunders / Elsevier, Philadelphia. 2008; Ch. 13.en_US
dc.identifier.citedreferenceElliott PM, Kindler H, Shah JS et al. Coronary microvascular dysfunction in male patients with Anderson–Fabry disease and the effect of treatment with alpha galactosidase A. Heart 2006; 92: 357 – 60.en_US
dc.identifier.citedreferenceMoore DF, Kaneski CR, Askari H, Schiffmann R. The cerebral vasculopathy of Fabry disease. J. Neurol. Sci. 2007; 257: 258 – 63.en_US
dc.identifier.citedreferenceGuo Z, Su W, Allen S et al. COX-2 up-regulation and vascular smooth muscle contractile hyperreactivity in spontaneous diabetic db/db mice. Cardiovasc. Res. 2005; 67: 723 – 35.en_US
dc.identifier.citedreferenceLinder AE, Weber DS, Whitesall SE, D’Alecy LG, Webb RC. Altered vascular reactivity in mice made hypertensive by nitric oxide synthase inhibition. J. Cardiovasc. Pharmacol. 2005; 46: 438 – 44.en_US
dc.identifier.citedreferencePannirselvam M, Verma S, Anderson TJ, Triggle CR. Cellular basis of endothelial dysfunction in small mesenteric arteries from spontaneously diabetic (db/db −/– ) mice: Role of decreased tetrahydrobiopterin bioavailability. Br. J. Pharmacol. 2002; 136: 255 – 63.en_US
dc.identifier.citedreferencePannirselvam M, Wiehler WB, Anderson T, Triggle CR. Enhanced vascular reactivity of small mesenteric arteries from diabetic mice is associated with enhanced oxidative stress and cyclooxygenase products. Br. J. Pharmacol. 2005; 144: 953 – 60.en_US
dc.identifier.citedreferenceShepherd JT, Katusic ZS. Endothelium-derived vasoactive factors. I. Endothelium-dependent relaxation. Hypertension 1991; 18 ( Suppl. III ): III - 76 – 85.en_US
dc.identifier.citedreferenceShu L, Shayman JA. Caveolin-associated accumulation of globotriaosylceramide in the vascular endothelium of alpha-galactosidase A null mice. J. Biol. Chem. 2007; 282: 20 960 – 7.en_US
dc.identifier.citedreferenceShu L, Lee L, Shayman JA. Regulation of phospholipase C-gamma activity by glycosphingolipids. J. Biol. Chem. 2002; 277: 18 447 – 53.en_US
dc.identifier.citedreferenceShu L, Shayman JA. Src kinase mediates the regulation of phospholipase C-gamma activity by glycosphingolipids. J. Biol. Chem. 2003; 278: 31 419 – 25.en_US
dc.identifier.citedreferenceBrown DA, London E. Structure and function of sphingolipid- and cholesterol-rich membrane rafts. J. Biol. Chem. 2000; 275: 17 221 – 4.en_US
dc.identifier.citedreferenceVanhoutte PM, Feletou M, Taddei S. Endothelium-dependent contractions in hypertension. Br. J. Pharmacol. 2005; 144: 449 – 58.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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