PMID- 20299683 OWN - NLM STAT- MEDLINE DCOM- 20100603 LR - 20181113 IS - 1524-4636 (Electronic) IS - 1079-5642 (Print) IS - 1079-5642 (Linking) VI - 30 IP - 6 DP - 2010 Jun TI - Monocyte chemoattractant protein-1 deficiency protects against visceral fat-induced atherosclerosis. PG - 1151-8 LID - 10.1161/ATVBAHA.110.205914 [doi] AB - OBJECTIVE: To determine the role of monocyte chemoattractant protein-1 (Mcp-1) on the progression of visceral fat-induced atherosclerosis. METHODS AND RESULTS: Visceral fat inflammation was induced by transplantation of perigonadal fat. To determine whether recipient Mcp-1 status affected atherosclerosis induced by inflammatory fat, apolipoprotein E-deficient (ApoE(-/-)) and ApoE(-/-) and Mcp-1-deficient (Mcp-1(-/-)) mice underwent visceral fat transplantation. Intravital microscopy was used to study leukocyte-endothelial interactions. To study the primary tissue source of circulating Mcp-1, both fat and bone marrow transplantation experiments were used. Transplantation of visceral fat increased atherosclerosis in ApoE(-/-) mice but had no effect on atherosclerosis in ApoE(-/-),Mcp-1(-/-) mice. Intravital microscopy revealed increased leukocyte attachment to the endothelium in ApoE(-/-) mice compared with ApoE(-/-),Mcp-1(-/-) mice after receiving visceral fat transplants. Transplantation of visceral fat increased plasma Mcp-1, although donor adipocytes were not the source of circulating Mcp-1 because no Mcp-1 was detected in plasma from ApoE(-/-),Mcp-1(-/-) mice transplanted with Wt fat, indicating that recipient Mcp-1-producing cells were affecting the atherogenic response to the fat transplantation. Consistently, transplantation of Mcp-1(-/-) fat to ApoE(-/-) mice did not lead to atheroprotection in recipient mice. Bone marrow transplantation between Wt and Mcp-1(-/-) mice indicated that the primary tissue source of circulating Mcp-1 was the endothelium. CONCLUSIONS: Recipient Mcp-1 deficiency protects against atherosclerosis induced by transplanted visceral adipose tissue. FAU - Ohman, Miina K AU - Ohman MK AD - Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-0644, USA. FAU - Wright, Andrew P AU - Wright AP FAU - Wickenheiser, Kevin J AU - Wickenheiser KJ FAU - Luo, Wei AU - Luo W FAU - Russo, Hana M AU - Russo HM FAU - Eitzman, Daniel T AU - Eitzman DT LA - eng GR - P01 HL057346/HL/NHLBI NIH HHS/United States GR - R01 HL073150-06A2/HL/NHLBI NIH HHS/United States GR - R01 HL073150/HL/NHLBI NIH HHS/United States GR - HL57346/HL/NHLBI NIH HHS/United States GR - HL073150/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20100318 PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (Apolipoproteins E) RN - 0 (Ccl2 protein, mouse) RN - 0 (Chemokine CCL2) SB - IM MH - Adipocytes/immunology MH - Animals MH - Apolipoproteins E/deficiency/genetics MH - Atherosclerosis/genetics/immunology/metabolism/*prevention & control MH - Bone Marrow Transplantation MH - Cell Adhesion MH - Chemokine CCL2/blood/*deficiency/genetics MH - Disease Models, Animal MH - Endothelial Cells/*immunology MH - Intra-Abdominal Fat/*immunology/transplantation MH - Leukocytes/*immunology MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Mice, Knockout MH - Microscopy, Video MH - Panniculitis/complications/*immunology/metabolism MH - Time Factors PMC - PMC2874123 MID - NIHMS198595 EDAT- 2010/03/20 06:00 MHDA- 2010/06/04 06:00 PMCR- 2011/06/01 CRDT- 2010/03/20 06:00 PHST- 2010/03/20 06:00 [entrez] PHST- 2010/03/20 06:00 [pubmed] PHST- 2010/06/04 06:00 [medline] PHST- 2011/06/01 00:00 [pmc-release] AID - ATVBAHA.110.205914 [pii] AID - 10.1161/ATVBAHA.110.205914 [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 2010 Jun;30(6):1151-8. doi: 10.1161/ATVBAHA.110.205914. Epub 2010 Mar 18.