Role of LpL (Lipoprotein Lipase) in Macrophage Polarization In Vitro and In Vivo
| Autor: | Yunying Hu, Svetlana Bagdasarov, Jennifer Grossman, Ira J. Goldberg, Tessa J. Barrett, Lesley-Ann Huggins, Diego Scerbo, Namrata Gumaste, Stephanie S. Chiang, Hye Rim Chang, Tatjana Josefs, Edward A. Fisher |
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| Rok vydání: | 2019 |
| Předmět: |
Macrophage polarization
Inflammation Sensitivity and Specificity Mice In vivo medicine Animals Humans Macrophage Cells Cultured Myeloid Progenitor Cells Triglycerides Mice Knockout chemistry.chemical_classification Macrophages Role LPL - Lipoprotein lipase Fatty acid Metabolism Macrophage Activation Atherosclerosis In vitro Disease Models Animal Lipoprotein Lipase chemistry Biochemistry Hyperlipoproteinemia Type I lipids (amino acids peptides and proteins) medicine.symptom Cardiology and Cardiovascular Medicine |
| Zdroj: | Arteriosclerosis, Thrombosis, and Vascular Biology. 39:1967-1985 |
| ISSN: | 1524-4636 1079-5642 |
| DOI: | 10.1161/atvbaha.119.312389 |
| Popis: | Objective: Fatty acid uptake and oxidation characterize the metabolism of alternatively activated macrophage polarization in vitro, but the in vivo biology is less clear. We assessed the roles of LpL (lipoprotein lipase)-mediated lipid uptake in macrophage polarization in vitro and in several important tissues in vivo. Approach and Results: We created mice with both global and myeloid-cell specific LpL deficiency. LpL deficiency in the presence of VLDL (very low-density lipoproteins) altered gene expression of bone marrow–derived macrophages and led to reduced lipid uptake but an increase in some anti- and some proinflammatory markers. However, LpL deficiency did not alter lipid accumulation or gene expression in circulating monocytes nor did it change the ratio of Ly6C high /Ly6C low . In adipose tissue, less macrophage lipid accumulation was found with global but not myeloid-specific LpL deficiency. Neither deletion affected the expression of inflammatory genes. Global LpL deficiency also reduced the numbers of elicited peritoneal macrophages. Finally, we assessed gene expression in macrophages from atherosclerotic lesions during regression; LpL deficiency did not affect the polarity of plaque macrophages. Conclusions: The phenotypic changes observed in macrophages upon deletion of Lpl in vitro is not mimicked in tissue macrophages. |
| Databáze: | OpenAIRE |
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