DISTINCT EXPRESSION PATTERNS OF CD44 ISOFORMS DURING HUMAN LUNG DEVELOPMENT AND IN PULMONARY FIBROSIS

Citation
M. Kasper et al., DISTINCT EXPRESSION PATTERNS OF CD44 ISOFORMS DURING HUMAN LUNG DEVELOPMENT AND IN PULMONARY FIBROSIS, American journal of respiratory cell and molecular biology, 13(6), 1995, pp. 648-656
Citations number
39
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
13
Issue
6
Year of publication
1995
Pages
648 - 656
Database
ISI
SICI code
1044-1549(1995)13:6<648:DEPOCI>2.0.ZU;2-7
Abstract
The transmembrane glycoprotein CD44 represents a family of molecules, all encoded by one gene. The variability of the isoforms is generated by alternative splicing of the nuclear RNA. Apart from the abundant st andard form (CD44s), the variant isoforms (CD44v) are mostly restricte d to epithelia. The present study demonstrates the expression of CD44s and CD44v isoforms in embryonic and fetal lungs and in normal and pat hologically altered (pulmonary fibrosis after radio- or chemotherapy) human adult pulmonary tissues. Using double immunofluorescence and avi din biotin complex (ABC) techniques on paraffin sections, presence of CD44s and CD44v isoforms (CD44v4, CD44v6, CD44v9) has been analyzed. I n normal lung tissue, CD44s is present at the cell surface of alveolar macrophages, in some interstitial cells and in epithelial cells. It i s also present in epithelial and non-epithelial cells during lung deve lopment. CD44v isoforms containing exon v6 and v9 encoded epitopes are selectively detectable in normal epithelial cells with a strong basol ateral distribution pattern in the entire population of type II pneumo cytes and in basal cells of the bronchial epithelium. During developme nt exon v9 encoded isoforms appear at the pseudoglandular stage, where as CD44v6 has only been found at the saccular stage. Examination of 12 fibrotic lung samples has revealed major alterations in the CD44 expr ession in comparison to normal lung tissue. These changes include cyto plasmic deposits of CD44s in alveolar epithelial cells and reduced exp ression of the CD44v6 and CD44v9 isoforms in alveolar epithelial and b ronchial epithelial cells. The results suggest that CD44v isoforms may be utilized by type II pneumocytes in epithelial-mesenchymal interact ions and in the maintenance of the pulmonary histoarchitecture. Pathol ogic alterations in pulmonary fibrosis are accompanied by disruption o f the histoarchitecture and loss of CD44v isoforms.