Problems of High Altitude Medicine and Biology

  • Almaz Aldashev
  • Robert Naeije

Table of contents

  1. Front Matter
    Pages i-viii
  2. James S. Milledge
    Pages 1-9
  3. Andrew Peacock, Oleg Pak, David Welsh
    Pages 39-55
  4. Saadia Eddahibi, Bernadette Raffestin, Serge Adnot
    Pages 57-68
  5. Lan Zhao, Francis Bahaa, Martin Wilkins
    Pages 69-86
  6. Akio Sakai, Ishizaki Takeshi, Koizumi Tomonobu, Matsumoto Takayuki
    Pages 101-117
  7. Annalisa Cogo, Federica Campigotto, Valter Fasano, Giovanni Grazzi
    Pages 119-131
  8. Baktybek K. Kojonazarov, Mirsaid M. Mirrakhimov, Nicholas W. Morrell, Martin R. Wilkins, Almaz Aldashev
    Pages 133-143
  9. Peter Bärtsch, Christoph Dehnert, Heimo Mairbäurl, Marc Moritz Berger
    Pages 185-195
  10. Sandrine Huez, Robert Naeije, Vitalie Faoro
    Pages 221-229
  11. T. M. Sooronbaev, S. B. Shabykeeva, A. K. Mirzaachmatova, G. K. Kadyraliev, Mirsaid M. Mirrakhimov
    Pages 249-257

About these proceedings

Introduction

The major characteristic pathological findings of pulmonary vascular remodelling are increased wall thickening of pulmonary vessels and mus- larization of small arteries. In laboratory animals, decreased ambient oxygen concentrations cause similar pathological findings, including pulmonary smooth muscle hypertrophy and proliferation [22,23]. It has been suggested that proliferation of pulmonary arterial smooth muscle cells (PASMC) is a key component of pulmonary vascular remodelling, and several in vitro studies have also addressed that exposure to hypoxia can stimulate prolife- tion of PASMC [13,4,1]. The proliferation of the PASMC begins when the cells enter into the cell cycle. The most important molecular event necessary for the progress of the cell cycle is phosphorylation of retinoblastoma protein by cyclin-dependent kinase (CDK)-cyclin complexes. The CDK activity can be inhibited by CDK inhibitors and the expression of CDK inhibitor is a major regulator of the transition between each phase of the cell cycle [7]. Previous studies have noted that CDK inhibitor p27 plays an important role in the inhibition of the CDK activity and proliferation in vascular smooth muscle cells [2,3]. The G1 phase in severe hypoxia is suggested to involve the CKI p27, because the expression of p27 increased in several cell-lines when they were exposed to extreme hypoxia [20,5]. Previous reports indicate that hypoxia decreases the p27 expression in the murine lung [23,24] and we found that PGI2 suppresses hypox- induced proliferation of PASMC and maintains p27 in PASMC [20].

Keywords

Atmen Biology Chemistry NATO Radiologieinformationssystem Science Security Sub-Series A hypertension

Editors and affiliations

  • Almaz Aldashev
    • 1
  • Robert Naeije
    • 2
  1. 1.Kirghiz Institute of CardiologyKyrgyz Republic
  2. 2.Free University of BrusselsBelgium

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4020-6300-8
  • Copyright Information Springer 2007
  • Publisher Name Springer, Dordrecht
  • eBook Packages Mathematics and Statistics
  • Print ISBN 978-1-4020-6299-5
  • Online ISBN 978-1-4020-6300-8
  • About this book