| First Author | Li J | Year | 2005 |
| Journal | Cell Cycle | Volume | 4 |
| Issue | 11 | Pages | 1599-607 |
| PubMed ID | 16205123 | Mgi Jnum | J:328817 |
| Mgi Id | MGI:7338894 | Doi | 10.4161/cc.4.11.2117 |
| Citation | Li J, et al. (2005) Impaired phagocytosis in caveolin-1 deficient macrophages. Cell Cycle 4(11):1599-607 |
| abstractText | 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 gamma-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. |
