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Title: Nestin(+) cells direct inflammatory cell migration in atherosclerosis.
Authors: Del Toro, Raquel
Chèvre, Raphael
Rodríguez, Cristina
Ordóñez, Antonio
Martínez-González, José
Andrés, Vicente
Méndez-Ferrer, Simón
metadata.dc.subject.mesh: Animals
Apolipoproteins E
Cell Movement
Chemokine CCL2
Diet, High-Fat
Endothelial Cells
Mice, Inbred C57BL
Mice, Knockout
Plaque, Atherosclerotic
Issue Date: 2-Sep-2016
Abstract: Atherosclerosis is a leading death cause. Endothelial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchymal cells contribute to this process. Bone marrow (BM) nestin(+) cells cooperate with endothelial cells in directing monocyte egress to bloodstream in response to infections. However, it remains unknown whether nestin(+) cells regulate inflammatory cells in chronic inflammatory diseases, such as atherosclerosis. Here, we show that nestin(+) cells direct inflammatory cell migration during chronic inflammation. In Apolipoprotein E (ApoE) knockout mice fed with high-fat diet, BM nestin(+) cells regulate the egress of inflammatory monocytes and neutrophils. In the aorta, nestin(+) stromal cells increase ∼30 times and contribute to the atheroma plaque. Mcp1 deletion in nestin(+) cells-but not in endothelial cells only- increases circulating inflammatory cells, but decreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification. Therefore, nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.
metadata.dc.identifier.doi: 10.1038/ncomms12706
Appears in Collections:Producción 2020

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