Am. J. Respir. Crit. Care Med., Vol 152, No. 6, Dec 1995, 2084-2089.
Localization of platelet-derived growth factor and insulin-like growth factor I in the fibrotic lung
S Homma, I Nagaoka, H Abe, K Takahashi, K Seyama, T Nukiwa and S Kira
Department of Respiratory Medicine, Juntendo University School of Medicine, Tokyo, Japan.
To better understand the mechanisms responsible for the increase in numbers
of fibroblasts and increased collagen synthesis in fibrotic intestitial
lung diseases, platelet-derived growth factor (PDGF)-A and PDGF-B, PDGF
receptor-alpha and -beta, insulin-like growth factor I (IGF-I), and IGF-I
receptor were evaluated immunohistochemically. Additionally, the messenger
ribonucleic acids (mRNAs) for PDGF-A and PDGF-B, PDGF receptor-alpha and
-beta, and IGF-I were investigated by in situ hybridization in alveolar
macrophages and lung tissues from patients with interstitial lung disease.
In specimens of bronchoalveolar lavage fluid (BALF), PDGF-A, PDGF-B, and
IGF-I were local in alveolar macrophages in patients with idiopathic
pulmonary fibrosis (IPF), patients with sarcoidosis (Sar), and normal
individuals. Although there were no differences between IPF and Sar in
terms of the staining intensity or number of positive cells, the number of
such cells was smaller in the normal controls. In lung tissues with
early-stage IPF, PDGF and IGF-I proteins were localized exclusively in
alveolar macrophages, mononuclear phagocytes, fibroblasts, alveolar Type II
cells, vascular endothelial cells, and vascular smooth-muscle cells. In
lung tissues with late-stage IPF and those from normal controls, only
alveolar macrophages contained PDGF and IGF-I proteins. Interestingly, the
cellular localizations of PDGF receptor-alpha and - beta, and of IGF-I
receptor were the same as those of the PDGF and IGF- I proteins in
early-stage IPF, whereas these cells were not positive for any of these
substances in late-stage IPF or normal controls.(ABSTRACT TRUNCATED AT 250
WORDS)
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Copyright © 1995 American Thoracic Society
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