Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Maria Gomez

Maria Gomez

Professor

Maria Gomez

Upregulated TRPC1 Channel in Vascular Injury In Vivo and Its Role in Human Neointimal Hyperplasia.

Author

  • B Kumar
  • Karl Dreja
  • S Shah
  • A Cheong
  • S-Z Xu
  • P Sukumar
  • J Naylor
  • A Forte
  • M Cipollaro
  • D McHugh
  • P A Kingston
  • A M Heagerty
  • C M Munsch
  • Andreas Bergdahl
  • Anna Hultgårdh
  • Maria Gomez
  • K E Porter
  • Per Hellstrand
  • D J Beech

Summary, in English

Occlusive vascular disease is a widespread abnormality leading to lethal or debilitating outcomes such as myocardial infarction and stroke. It is part of atherosclerosis and is evoked by clinical procedures including angioplasty and grafting of saphenous vein in bypass surgery. A causative factor is the switch in smooth muscle cells to an invasive and proliferative mode, leading to neointimal hyperplasia. Here we reveal the importance to this process of TRPC1, a homolog of Drosophila transient receptor potential. Using 2 different in vivo models of vascular injury in rodents we show hyperplasic smooth muscle cells have upregulated TRPC1 associated with enhanced calcium entry and cell cycle activity. Neointimal smooth muscle cells after balloon angioplasty of pig coronary artery also express TRPC1. Furthermore, human vein samples obtained during coronary artery bypass graft surgery commonly exhibit an intimal structure containing smooth muscle cells that expressed more TRPC1 than the medial layer cells. Veins were organ cultured to allow growth of neointimal smooth muscle cells over a 2-week period. To explore the functional relevance of TRPC1, we used a specific E3-targeted antibody to TRPC1 and chemical blocker 2-aminoethoxydiphenyl borate. Both agents significantly reduced neointimal growth in human vein, as well as calcium entry and proliferation of smooth muscle cells in culture. The data suggest upregulated TRPC1 is a general feature of smooth muscle cells in occlusive vascular disease and that TRPC1 inhibitors have potential as protective agents against human vascular failure.

Department/s

  • Vascular Physiology
  • Vessel Wall Biology

Publishing year

2006

Language

English

Pages

557-563

Publication/Series

Circulation Research

Volume

98

Issue

4

Document type

Journal article

Publisher

American Heart Association

Topic

  • Cardiac and Cardiovascular Systems

Keywords

  • neointimal hyperplasia
  • transient receptor potential
  • calcium channel
  • vascular smooth muscle cells

Status

Published

Research group

  • Vascular Physiology
  • Vessel Wall Biology

ISBN/ISSN/Other

  • ISSN: 0009-7330