Abstract
Caveolae are plasma membrane invaginations that function as important regulators of numerous cellular processes, including signal transduction, cholesterol trafficking, and endocytosis. Caveolin-1 (Cav-1) constitutes the main structural protein of caveolae membranes. Here, we report an in vivo increase in the number of apoptotic cells in the thymus and spleen of Cav-1 deficient mice, following whole-body γ-irradiation. We demonstrate that this increase in apoptotic cells is not due to increased apoptosis in lymphocytes per se, which normally do not express Cav-1, but rather to the decreased phagocytic clearance of apoptotic cells by macrophages, which do express Cav-1. Utilizing in vitro phagocytosis assays of both apoptotic thymocytes and Escherichia coli K-12 BioParticles, we demonstrate that the loss of Cav-1 decreases the phagocytic ability of thioglycollate-elicited peritoneal macrophages. We suggest that impaired macrophage phagocytosis in Cav-1 knockout mice could have implications for altered innate immunity against pathogens, the regulation of inflammatory responses, and the development of autoimmune disease.
Original language | English (US) |
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Pages (from-to) | 1599-1607 |
Number of pages | 9 |
Journal | Cell Cycle |
Volume | 4 |
Issue number | 11 |
DOIs | |
State | Published - Nov 2005 |
Keywords
- Apoptosis
- Autoimmune disease
- Caveolae
- Caveolin-1
- Innate immunity
- Macrophage
- Phagocytosis
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology