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Impaired phagocytosis of apoptotic cells causes accumulation of bone marrow-derived macrophages in aged mice
Ok-Hee Kim1, Hyojung Kim1, Jinku Kang1, Dongki Yang2, Yu-Hoi Kang3, Dae Ho Lee1, Gi Jeong Cheon4, Sang Chul Park5, BYUNG-CHUL OH1,2,*
1Lee Gil Ya Cancer and Diabetes Institute, and 2Department of physiology, College of Medicine, Gachon University, Incheon 21999, Korea,
3Samsung advanced institute of technology,, Samsung electronics Co. Ltd. Korea,
4Department of Nuclear Medicine,, Seoul National University College of Medicine, Seoul, Korea,
5Well aging research center,, DGIST, Daegu 42988, Korea
Abstract
Accumulation of tissue macrophages is a significant characteristic of disease-associated chronic inflammation, and facilitates the progression of disease pathology. However, the functional roles of these bone marrow-derived macrophages (BMDMs) in aging are unclear. Here, we identified age-dependent macrophage accumulation in the bone marrow, showing that aging significantly increases the number of M1 macrophages and impairs polarization of BMDMs. We found that age-related dysregulation of BMDMs is associated with abnormal overexpression of the anti-inflammatory interleukin-10. BMDM dysregulation in aging impairs the expression levels of pro-inflammatory cytokines and genes involved in B-cell maturation and activation. Phagocytosis of apoptotic Jurkat cells by BMDMs was reduced because of low expression of phagocytic receptor CD14, indicating that increased apoptotic cells may result from defective phagocytosis of apoptotic cells in the BM of aged mice. Therefore, CD14 may represent a promising target for preventing BMDM dysregulation, and macrophage accumulation may provide diagnostic and therapeutic clues.
Abstract, Accepted Manuscript(in press) [Submitted on September 29, 2016, Accepted on November 14, 2016]
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