HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Nagai, K. Articles by Nishimura, M. Search for Related Content PubMed PubMed Citation Articles by Nagai, K. Articles by Nishimura, M.

Decrease of vascular endothelial growth factor in macrophages from long-term smokers

First Dept of Medicine, Hokkaido University School of Medicine, Sapporo, Japan

CORRESPONDENCE: T. Betsuyaku, First Dept of Medicine, Hokkaido University School of Medicine, N-15, W-7, Kita-ku, Sapporo, Japan, 060-8638. Fax: 81 117067899. E-mail: bytomoko@med.hokudai.ac.jp

Keywords: Ageing, apoptosis, bronchoalveolar lavage, chronic obstructive pulmonary disease, emphysema, smoking

Received: September 24, 2004
Accepted December 6, 2004

Vascular endothelial growth factor (VEGF), a survival factor for endothelial cells and a promoter of angiogenesis, is reportedly expressed in alveolar macrophages (AMs).

To investigate whether long-term smoking with age affects VEGF expression in AMs, bronchoalveolar lavage (BAL) was performed on 18 young and 23 older volunteers with various smoking histories. The expressions of VEGF and its functional receptor, fms-like tyrosine kinase (Flt)-1, were quantified in AMs by real-time RT-PCR and, further, the level of VEGF in BAL fluid was determined by ELISA.

VEGF mRNA in AMs demonstrated a 1.8-fold reduction in current smokers compared with nonsmokers in older subjects and, furthermore, a 1.5-fold downregulation in those with emphysema, although there was no difference between current smokers and nonsmokers among the young subjects. The downregulation in total VEGF mRNA was supported by the substantial reduction of VEGF121 and VEGF165 isoforms. However, in contrast, Flt-1 mRNA did not differ within the older groups, whereas it was upregulated in young current smokers compared with age-matched nonsmokers. VEGF in BAL fluid is significantly decreased in current smokers compared with nonsmokers, regardless of their age.

In conclusion, these data imply that the biological availability of vascular endothelial growth factor in alveolar macrophages is impaired in older current smokers with long-term smoking histories.

This article has been cited by other articles:

				T. Kinnaird, E. Stabile, S. Zbinden, M.-S. Burnett, and S. E. Epstein Cardiovascular risk factors impair native collateral development and may impair efficacy of therapeutic interventions Cardiovasc Res, May 1, 2008; 78(2): 257 - 264. [Abstract] [Full Text] [PDF]

				J. A. Elias, M. J. Kang, K. Crouthers, R. Homer, and C. G. Lee State of the Art. Mechanistic Heterogeneity in Chronic Obstructive Pulmonary Disease: Insights from Transgenic Mice Proceedings of the ATS, August 1, 2006; 3(6): 494 - 498. [Abstract] [Full Text] [PDF]

				K Nagai, T Betsuyaku, T Kondo, Y Nasuhara, and M Nishimura Long term smoking with age builds up excessive oxidative stress in bronchoalveolar lavage fluid Thorax, June 1, 2006; 61(6): 496 - 502. [Abstract] [Full Text] [PDF]