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Marsh, LM; Cakarova, L; Kwapiszewska, G; von Wulffen, W; Herold, S; Seeger, W; Lohmeyer, J.
Surface expression of CD74 by type II alveolar epithelial cells: a potential mechanism for macrophage migration inhibitory factor-induced epithelial repair.
Am J Physiol Lung Cell Mol Physiol. 2009; 296(3): L442-L452. Doi: 10.1152/ajplung.00525.2007 [OPEN ACCESS]
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Leading authors Med Uni Graz: Marsh Leigh
Co-authors Med Uni Graz: Kwapiszewska-Marsh Grazyna
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Abstract:: Macrophage migration inhibitory factor (MIF) is a pleiotropic proinflammatory cytokine involved in acute lung injury and other processes such as wound repair and tumor growth. MIF exerts pro-proliferative effects on a variety of cell types including monocytes/macrophages, B cells, and gastric epithelial cell lines through binding to the major histocompatibility complex type II-associated invariant chain, CD74. In acute lung injury, inflammatory damage of the alveolar epithelium leads to loss of type I alveolar epithelial cells (AEC-I), which are replaced by proliferation and differentiation of type II alveolar epithelial cells (AEC-II). In this study we have investigated the potential of MIF to contribute to alveolar repair by stimulating alveolar epithelial cell proliferation. We show that murine AEC-II, but not AEC-I, express high surface levels of CD74 in vivo. Culture of AEC-II in vitro resulted in decreased mRNA levels for CD74 and loss of surface CD74 expression, which correlated with a transition of AEC-II to an AEC-I-like phenotype. MIF stimulation of AEC-II induced rapid and prolonged phosphorylation of ERK1/2 and Akt, increased expression of cyclins D1 and E, as well as AEC-II proliferation. Corresponding MIF signaling and enhanced thymidine incorporation was observed after MIF stimulation of MLE-12 cells transfected to overexpress CD74. In contrast, MIF did not induce MAPK activation, gene transcription, or increased proliferation in differentiated AEC-I-like cells that lack CD74. These data suggest a previously unidentified role of MIF-CD74 interaction by inducing proliferation of AEC-II, which may contribute to alveolar repair.
Find related publications in this database (using NLM MeSH Indexing): Acute Lung Injury - genetics Acute Lung Injury - immunology Acute Lung Injury - pathology Acute Lung Injury - physiopathology; Animals -; Antigens, Differentiation, B-Lymphocyte - genetics Antigens, Differentiation, B-Lymphocyte - metabolism; Base Sequence -; Cell Differentiation -; Cell Proliferation -; Cells, Cultured -; DNA Primers - genetics; Epithelial Cells - classification Epithelial Cells - cytology Epithelial Cells - immunology; Histocompatibility Antigens Class II - genetics Histocompatibility Antigens Class II - metabolism; Macrophage Migration-Inhibitory Factors - pharmacology Macrophage Migration-Inhibitory Factors - physiology; Mice -; Mice, Inbred C57BL -; Peptides - metabolism; Phenotype -; Pulmonary Alveoli - cytology Pulmonary Alveoli - immunology; Signal Transduction -; Transfection -
Find related publications in this database (Keywords): lung; epithelial proliferation; resolution of inflammation; macrophage migration inhibitory factor