M Kasper, U Gunthert, P Dall, K Kayser, D Schuh, G Haroske and M Muller
Institute of Pathology, Technical University of Dresden, Germany.

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 standard form (CD44s), the variant isoforms (CD44v) are mostly restricted to epithelia. The present study demonstrates the expression of CD44s and CD44v isoforms in embryonic and fetal lungs and in normal and pathologically altered (pulmonary fibrosis after radio- or chemotherapy) human adult pulmonary tissues. Using double immunofluorescence and avidin biotin complex (ABC) techniques on paraffin sections, presence of CD44s and CD44v isoforms (CD44v4, CD44v6, CD44v9) has been analyzed. In normal lung tissue, CD44s is present at the cell surface of alveolar macrophages, in some interstitial cells and in epithelial cells. It is also present in epithelial and non-epithelial cells during lung development. CD44v isoforms containing exon v6 and v9 encoded epitopes are selectively detectable in normal epithelial cells with a strong basolateral distribution pattern in the entire population of type II pneumocytes and in basal cells of the bronchial epithelium. During development exon v9 encoded isoforms appear at the pseudoglandular stage, whereas CD44v6 has only been found at the saccular stage. Examination of 12 fibrotic lung samples has revealed major alterations in the CD44 expression in comparison to normal lung tissue. These changes include cytoplasmic deposits of CD44s in alveolar epithelial cells and reduced expression of the CD44v6 and CD44v9 isoforms in alveolar epithelial and bronchial epithelial cells. The results suggest that CD44v isoforms may be utilized by type II pneumocytes in epithelial-mesenchymal interactions and in the maintenance of the pulmonary histoarchitecture.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				G. Pacheco-Rodriguez, W. K. Steagall, D. M. Crooks, L. A. Stevens, H. Hashimoto, S. Li, J.-a. Wang, T. N. Darling, and J. Moss TSC2 Loss in Lymphangioleiomyomatosis Cells Correlated with Expression of CD44v6, a Molecular Determinant of Metastasis Cancer Res., November 1, 2007; 67(21): 10573 - 10581. [Abstract] [Full Text] [PDF]

				E. Vachon, R. Martin, J. Plumb, V. Kwok, R. W. Vandivier, M. Glogauer, A. Kapus, X. Wang, C.-W. Chow, S. Grinstein, et al. CD44 is a phagocytic receptor Blood, May 15, 2006; 107(10): 4149 - 4158. [Abstract] [Full Text] [PDF]

				B. Salaun, B. de Saint-Vis, N. Pacheco, Y. Pacheco, A. Riesler, S. Isaac, C. Leroux, V. Clair-Moninot, J.-J. Pin, J. Griffith, et al. CD208/Dendritic Cell-Lysosomal Associated Membrane Protein Is a Marker of Normal and Transformed Type II Pneumocytes Am. J. Pathol., March 1, 2004; 164(3): 861 - 871. [Abstract] [Full Text] [PDF]

				U. Uhlig, H. Fehrenbach, R. A. Lachmann, T. Goldmann, B. Lachmann, E. Vollmer, and S. Uhlig Phosphoinositide 3-OH Kinase Inhibition Prevents Ventilation-induced Lung Cell Activation Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 201 - 208. [Abstract] [Full Text] [PDF]

				H. Fehrenbach, A. Fehrenbach, T. Pan, M. Kasper, and R.J. Mason Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo Eur. Respir. J., November 1, 2002; 20(5): 1185 - 1197. [Abstract] [Full Text] [PDF]

				M. Silvestri, L. Fregonese, F. Sabatini, G. Dasic, and G.A. Rossi Fluticasone and salmeterol downregulate in vitro, fibroblast proliferation and ICAM-1 or H-CAM expression Eur. Respir. J., July 1, 2001; 18(1): 139 - 145. [Abstract] [Full Text] [PDF]

				Q. Yu and B. P. Toole A New Alternatively Spliced Exon between v9 and v10 Provides a Molecular Basis for Synthesis of Soluble CD44 J. Biol. Chem., August 23, 1996; 271(34): 20603 - 20607. [Abstract] [Full Text] [PDF]