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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Zhao, Juanjuan Migliorini, Mary Kann, Maricel G. Doughty, Emily K. Cao, Chunzhang Zhang, Li Strickland, Dudley K. |
| Description | Author Affiliation: Cao C ( From the Departments of Physiology and.); Zhao J ( From the Departments of Physiology and.); Doughty EK ( the Department of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland 21250.); Migliorini M ( Surgery, Center for Vascular and Inflammatory Diseases, the University of Maryland, School of Medicine, Baltimore, Maryland 21201 and.); Strickland DK ( Surgery, Center for Vascular and Inflammatory Diseases, the University of Maryland, School of Medicine, Baltimore, Maryland 21201 and.); Kann MG ( the Department of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland 21250.); Zhang L ( From the Departments of Physiology and lizhang@som.umaryland.edu.) |
| Abstract | Mac-1 exhibits a unique inhibitory activity toward IL-13-induced JAK/STAT activation and thereby regulates macrophage to foam cell transformation. However, the underlying molecular mechanism is unknown. In this study, we report the identification of IL-13R 1, a component of the IL-13 receptor (IL-13R), as a novel ligand of integrin Mac-1, using a co-evolution-based algorithm. Biochemical analyses demonstrated that recombinant IL-13R 1 binds Mac-1 in a purified system and supports Mac-1-mediated cell adhesion. Co-immunoprecipitation experiments revealed that endogenous Mac-1 forms a complex with IL-13R 1 in solution, and confocal fluorescence microscopy demonstrated that these two receptors co-localize with each other on the surface of macrophages. Moreover, we found that genetic inactivation of Mac-1 promotes IL-13-induced JAK/STAT activation in macrophages, resulting in enhanced polarization along the alternative activation pathway. Importantly, we observed that Mac-1(-/-) macrophages exhibit increased expression of foam cell differentiation markers including 15-lipoxygenase and lectin-type oxidized LDL receptor-1 both in vitro and in vivo. Indeed, we found that Mac-1(-/-)LDLR(-/-) mice develop significantly more foam cells than control LDLR(-/-) mice, using an in vivo model of foam cell formation. Together, our data establish for the first time a molecular mechanism by which Mac-1 regulates the signaling activity of IL-13 in macrophages. This newly identified IL-13R 1/Mac-1-dependent pathway may offer novel targets for therapeutic intervention in the future. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 35 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-08-28 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Interleukin-13 Receptor Alpha1 Subunit Metabolism Interleukin-13 Macrophage-1 Antigen Macrophages Animals Biological Markers Cell Differentiation Cell Membrane Cell Polarity Evolution, Molecular Foam Cells Cytology Gene Silencing Janus Kinases Mice, Inbred C57BL Protein Binding Recombinant Proteins STAT Transcription Factors Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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