| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 133, 193-203, Copyright © 1988 by American Society for Investigative Pathology
REGULAR ARTICLES |
K Adachi, K Yamauchi, JF Bernaudin, P Fouret, VJ Ferrans and RG Crystal
Pulmonary Branche, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
Populations of alveolar macrophages recovered from the lower respiratory tract secrete fibronectin, a multi-functional glycoprotein capable of influencing cell migration, attachment, differentiation, and proliferation. Using in situ hybridization of 35S-labeled antisense and sense RNA fibronectin probes, the present study demonstrates that most, but not all, normal alveolar macrophages contain fibronectin mRNA transcripts, and that among those macrophages expressing this gene, the relative amount of fibronectin mRNA transcripts varies from cell to cell. Interestingly, while 66 +/- 3% of normal alveolar macrophages contain fibronectin mRNA transcripts, this is increased to 82 +/- 2% (P less than 0.01) of alveolar macrophages recovered from the lungs of individuals with idiopathic pulmonary fibrosis (IPF), a chronic inflammatory disorder associated with exaggerated amounts of fibronectin in the lower respiratory tract. Furthermore, of the macrophages expressing the fibronectin gene, those from IPF patients contain more fibronectin mRNA transcripts than those from normals. Consistent with this observation, evaluation of tissue samples from IPF patients demonstrated that of all cells present, alveolar macrophages showed the greatest numbers of fibronectin mRNA transcripts per cell. These observations demonstrate that there can be marked cell-to-cell variation in the expression of the gene for a macrophage product such as fibronectin, suggesting that there are processes that modulate similar cells in the same anatomic compartment to vary their expression of the same gene.
This article has been cited by other articles:
![]() |
E. M. Pierce, K. Carpenter, C. Jakubzick, S. L. Kunkel, K. R. Flaherty, F. J. Martinez, and C. M. Hogaboam Therapeutic Targeting of CC Ligand 21 or CC Chemokine Receptor 7 Abrogates Pulmonary Fibrosis Induced by the Adoptive Transfer of Human Pulmonary Fibroblasts to Immunodeficient Mice Am. J. Pathol., April 1, 2007; 170(4): 1152 - 1164. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. J. Tom, C. M. Doller, A. T. Malouf, and J. Silver Astrocyte-Associated Fibronectin Is Critical for Axonal Regeneration in Adult White Matter J. Neurosci., October 20, 2004; 24(42): 9282 - 9290. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. WEITKAMP, P. CULLEN, G. PLENZ, H. ROBENEK, and J. RAUTERBERG Human macrophages synthesize type VIII collagen in vitro and in the atherosclerotic plaque FASEB J, August 1, 1999; 13(11): 1445 - 1457. [Abstract] [Full Text] |
||||
![]() |
J. J. Avila, P. A. Lympany, P. Pantelidis, K. I. Welsh, C. M. Black, and R. M. du Bois Fibronectin Gene Polymorphisms Associated with Fibrosing Alveolitis in Systemic Sclerosis Am. J. Respir. Cell Mol. Biol., January 1, 1999; 20(1): 106 - 112. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |