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Lipoprotein Lipase Affects Macrophage Content and Phenotype in Aorta and Adipose Tissue
Author(s) -
Chang Chuchun Liz,
GarciaArco Itsaso,
Kim Ji Young,
Goldberg Ira J,
Deckelbaum Richard J
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.46.1
Subject(s) - adipose tissue , lipoprotein lipase , medicine , endocrinology , inflammation , adipose tissue macrophages , stromal cell , immune system , bone marrow , chemistry , biology , white adipose tissue , immunology
Macrophages (Mq) link inflammation to atherogenesis and insulin resistance. We have reported that dietary n‐3 fatty acids decrease arterial lipoprotein lipase (LpL) and Mq. We now questioned whether LpL can direct tissue Mq trafficking. Transgenic LpL knockout mice rescued with muscle LpL expression (MCKL0) and MCKL0 transplanted with bone marrow (BM) w/ or w/o LpL expression were used to study Mq in aorta and adipose tissue. Immune cells and interacting factors were examined by immunofluorescence, RT‐PCR, or flow cytometry. LpL deletion reduced arterial Mq by >; 30%, which was restored by reconstitution of LpL‐expressing BM. By contrast, in adipose tissue, MCKL0 had a 50% increase in Mq content and >; 5‐fold increase in expression of chemotactic MCP‐1/CCR‐2 and anti‐inflammatory M2 markers (p<0.05). Interestingly, increased Mq‐associated markers were found in adipose tissue and adipocytes, but not in stromal vascular cells, in MCKL0. In blood, MCKL0 have total leukocytes, neutrophils and monocytes ~ 40% lower than control (p<0.05). Inflammatory Gr‐1hi monocytes were decreased by 25%, whereas Gr‐1lo monocytes were increased by 2 fold, in MCKL0 (p<0.05). These data suggest that LpL affects local Mq content and phenotype, in part, via altering immune cell profiling. In the absence of LpL, we hypothesize that a self‐adaptive mechanism that causes adipocytes to produce pro‐inflammatory mediators might exist. Grant Funding Source : NIH‐HL40404 (RJD); T32‐ DK007674 /HL007343 (CLC)