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This Article Full Text Full Text (PDF) All Versions of this Article: 289/3/L382    most recent 00476.2004v1 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 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 Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Clegg, G. R. Articles by McElroy, M. C. Search for Related Content PubMed PubMed Citation Articles by Clegg, G. R. Articles by McElroy, M. C.

Coexpression of RTI₄₀ with alveolar epithelial type II cell proteins in lungs following injury: identification of alveolar intermediate cell types

¹Edinburgh Medical Research Council Centre for Inflammation Research, University of Edinburgh, Scotland, United Kingdom; and ²University of Pennsylvania Medical Center, Pulmonary, Allergy, and Critical Care Division, Philadelphia, Pennsylvania

Submitted 30 December 2004 ; accepted in final form 17 April 2005

Injured alveolar epithelial type (AT) I cells are replaced following the proliferation and transformation of ATII cells to new ATI cells. RTI₄₀ is an ATI cell-specific protein required for normal lung development. We hypothesized that intermediate cell types in the ATII-to-ATI cell transformation would coexpress RTI₄₀ and ATII cell-selective proteins. To test this hypothesis, we used a rat model of Staphylococcus aureus-induced acute lung injury and a panel of ATI and ATII cell-specific and -selective antibodies. S. aureus induced an acute inflammatory reaction that was resolving by day 3 postinoculation. At day 3 postinoculation, the alveolar wall was thickened secondary to ATII cell hyperplasia. With the use of confocal microscopy, there was a fivefold increase in the fractional surface area of alveolar walls stained with ATII cell membrane proteins (RTII₇₀ and MMC4) and a decrease in the fractional surface area associated with RTI₄₀-expressing cells. S. aureus-treated lungs also contained unique cell types that coexpressed the RTI₄₀ and ATII markers RTI₄₀/MMC4/RTII₇₀- and RTI₄₀/MMC4-positive cells. These cells were not observed in control lungs. RTI₄₀/MMC4-positive cells were also found in cultured ATII cells before they transformed to an ATI-like phenotype. Our data suggest that RTI₄₀/MMC4/RTII₇₀- and RTI₄₀/MMC4-positive cells are intermediates in the ATII-to-ATI cell transformation. These data also suggest that the coexpression of RTI₄₀ with ATII cell proteins may be used to identify and investigate ATII cell transdifferentiation to ATI cells following injury.

Staphylococcus aureus; aquaporin-5; MMC4 antigen

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