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1996 Fiscal Year Final Research Report Summary

A Bio-Engineering Approach to Endothelial Cell Signal Transduction and Responses to Fluid Shear Stress

Research Project

Project/Area Number 07408036
Research Category

Grant-in-Aid for Scientific Research (A)

Allocation TypeSingle-year Grants
Section一般
Research Field Biomedical engineering/Biological material science
Research InstitutionUniversity of Tokyo

Principal Investigator

KAMIYA Akira  University of Tokyo, Institute of Medical Electronics, Faculty of Medicine, Professor, 医学部, 教授 (50014072)

Co-Investigator(Kenkyū-buntansha) ANDO Joji  University of Tokyo, Dept, of Cardiovascular Biomechanics, Faculty of Medicine,, 医学部, 客員助教授 (20159528)
Project Period (FY) 1995 – 1996
KeywordsSHEAR STRESS / ENDOTHELIAL CELL / CALCIUM ION / VCAM-1 / ADHESION MOLECULE / BLOOD FLOW / HEMODYNAMIC FORCE / VCAM-1
Research Abstract

We applied controlled levels of fluid shear stress to cultured endothelial cells (ECs) in a specially designed flow-loading chamber, and examined the changes in intracellular Ca^<2+> concentrations ([Ca^<2+>]) and adhesion molecule expressions.
When subjected to shear stress in the presence of extracellular ATP,ECs showed the increase in [Ca^<2+>]. Different patterns including peak & plateau, oscillation, and transient were observed in individual cells. The percentage of the pattern was 62%, 32%and6%, respectively. Regardless of the patterns, [Ca^<2+>] increase initiated from specific loci at cell edges, and propagated through the entire cell body as a Ca^<2+> wave. The loci corresponded to the caveolin-rich in ECs, suggesting that the information of shear stress enters via caveolae.
Shear stress inhibited the cell surface expression of vascular adhesion molecule-1 (VCAM-1) in mouse lymphnode venule ECs, and simultaneously decreased the mRNA levels. The decrease in mRNA levels was due to the suppression of VCAM-1 gene transcription, and double AP1 consensus elements in VCAM-1 promoter was essential for the shear-induced suppression of transcriptional activity. This is a negative shear stress responsive element, which was first demonstrated by this study.

  • Research Products

    (16 results)

All Other

All Publications (16 results)

  • [Publications] J.Ando: "Differential displav and cloning of shear stress-responsive messenger RNAs in human endothelial cells." Biochem.Boiphys.Res.Commun.225. 347-351 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Y.Wang: "Contribution of sustained Ca^<2+> elevation for nitric oxide production in endothelial cells and subsequent modulation of Ca^<2+> transient in vascular smooth muscle cells" J.Biol.Chem.271. 5647-5655 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] H.Tsuboi: "Flow stimulates ICAM-1 expression time-and shear stress-dependently in human endothelial cells." Biochem.Boiphys.Res.Commun.206. 988-996 (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Y.Takada: "Fluid shear stress increases the expression of thrombomodulin by cultured human endothelial cells." Biochem.Boiphys.Res.Commun.205. 1345-1352 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] W.Yang: "Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells." Biochem.Boiphys.Res.Commun.203. 1160-1167 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] J.Ando: "Shear stress inhibits the adhesion of cultured mouse endothelial cells to lymphocytes by down-regulating VCAM-1 expression." Am.J.Physiol.267. C679-C687 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] J.Ando: "Fluid shear stress differentialy modulates adhesion molecule expression in human vascular endothelial cells. In "Organ Microcirculation : Bridging between Basic and Clinical Sciences",M.Tshuchiya et al.eds.," Excerpta Medica,Tokyo, 8 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] J.Ando: "Flow-dependent regulation of gene expression in vascular endothelial cells." Jpn.Heart J., 14 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] J.Ando: "Differential display and cloning of shear stress-responsive messenger RNAs in human endothelial cells." Biochem. Biophys. Res. Commun.225. 347-351 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] W.Yang: "Contribution of sustained Ca^<2+> elevation for nitric oxide production in endothelial cells and subsequent modulation of Ca^<2+> transient in vascular smooth muscle cells in coculture." J.Biol. Chem.271. 5647-5655 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] H.Tsuboi: "Flow stimulates ICAM-1 expression time-and shear stress-dependently in human endothelial cells." Biochem. Biophys. Res. Commun.206. 988-996 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Y.Takeda: "Fluid shear stress increases the expression of thrombomodulin by cultured human endothelial cells." Biochem. Biophys. Res. Commun.205. 1345-1352 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] W.Yang: "Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells." Biochem. Biophys. Res. Commun.203. 1160-1167 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] J.Ando: "Shear stress inhibits the adhesion of cultured mouse endothelial cells to lymphocytes by down-regulating VCAM-1 expression." Am. J.Physiol.267. C679-C687 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] J.Ando: "Fluid shear stress differentialy modulates adhesion molecule expression in human vascular endothelial cells. In "Organ Microcirculation : Bridging between Basic and Clinical Sciences", M.Tshuchiya et al. eds." Excerpta Medica, Tokyo. 8. (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] J.Ando: "Flow-dependent regulation of gene expression in vascular endothelial cells." Jpn. Heart J.14. (1996)

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

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Published: 1999-03-09  

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