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1999 Fiscal Year Final Research Report Summary

Research on the role of angiotensinogen gene in the pathogenesis of essential hypertension

Research Project

Project/Area Number 10470504
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Human genetics
Research InstitutionASAHIKAWA MEDICAL COLLEGE

Principal Investigator

HATA Akira  ASAHIKAWA MEDICAL COLLEGE, PROFESSOR, 医学部, 教授 (00244541)

Co-Investigator(Kenkyū-buntansha) INOUE Ituro  THE INSTITUTE OF MEDICAL SCIENCE, THE UNIVERSITY OF TOKYO, ASSOCIATE PROFESSOR, 医科学研究所, 助教授 (00192500)
Project Period (FY) 1998 – 1999
Keywordsangiotensinogen / hypertension / salt / mouse / gene copy number
Research Abstract

1) In vivo expression of angiotensinogen gene (AGT) is different between T allele and M allele. We have previously demonstrated about 20% higher expression in T allele than in M allele by way of in vitro experiments. In this study, we have tried to show allele dependent higher expression of AGT in vivo. For this purpose, we collected human cardiac tissue obtained in the operation of coronary artery bypass grafting (CABG). Out of 64 samples, 11 samples were revealed from the patient whose genotype is heterozygous of M235T (MT type). With these 11 samples, we have performed allele specific expression assay with primer pairs of P^<32> end-labeled common and allele specific oligonucleotide primer and Taq DNA ligase. Densitometrically, we found AGT expression from T alleles were 0 to 20% higher than that from M allele. This result may indicate the higher expression of AGT could be the cause of hypertension susceptibility.
2) We tried to show the difference of salt sensitivity in mice whose number of AGT gene copies ranged from 1 to 4. As the developer of these mice claimed, we have observed copy number dependent increase of blood pressure. However, we could not detect significant difference of blood pressure between high salt load (8%) and low salt diet (0.6%) in any combination of mice. Two possibilities could be considered for our result. One could be due to tail-cuff method we employed to measure blood pressure. The other could be due to the mouse strain which may be salt insensitive.

  • Research Products

    (14 results)

All Other

All Publications (14 results)

  • [Publications] Oike Yet al.: "Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: Implication of a dominant negative mechanism."Hum.Mol Genet. 8. 387-396 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Oike Y et al.: "Mice homozygous for a truncated form of CREB-biding protein exhibit defects in hematopoiesis and vasculo Oangiogenesis."Blood. 93. 2771-2779 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Saito T et al.: "Immunohistochemical determination of Wilson Copper-transporting P-type ATPase in the brain tissues of the rat"Neuroscience. 266. 13-16 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kamigaki M et al.: "Familial hypercholesterolemia with cholesteryl ester transfer protein deficiency"Int Med. 37. 523-527 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kobashi G: "Association of a variant of the angiotensinogen gene with pure type of hypertension in pregnancy in the Japanese"Am J Med Genet. 86. 232-236 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hirayama H et al.: "Five familial hypercholesterolemic kindreds in Japan with novel mutations of the LDL receptor gene"J Hum Genet. 43. 250-254 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Okabe M et al.: "Relationship between Cu metabolism hereditary disorders and distribution of Cu-metallothionein in kidneys.Metallothionein IV"Birkhauser verlag Basel/Switherland. 413-419 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] 羽田 明: "高血圧.遺伝子治療開発ハンドブック"エヌ・ティー・エス. 92-95 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Oike Y et al.: "Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice : Implication of a dominant negative mechanism."Hum Mol Genet.. 8. 387-396 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Oike Y et al.: "Mice homozygous for a truncated form of CREB-binding protein exhibit defects in hemopoiesis and vasculoangiogenesis."Blood. 93. 2771-2779 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Saito T et al.: "Immunohistochemical determination of Wilson Copper-transporting P-type ATPase in the brain tissues of the rat."Neuroscience letters. 266. 13-16 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Kamigaki M et al.: "Familial hypercholesterolemia with cholesteryl ester transfer protein deficiency."Int Med.. 37. 523-527 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Kobashi G et al.: "Association of a variant of the angiotensinogen gene with pure type of hypertension in pregnancy in the Japanese."Am J Med Genet.. 86. 232-236 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Hirayama H et al.: "Five familial hypercholesterolemic kindreds in Japan with novel mutations of the LDL receptor gene."J Hum Genet.. 43. 250-254 (1998)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2002-03-26  

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