Nestin+ cells direct inflammatory cell migration in atherosclerosis

Raquel del Toro (), Raphael Chèvre, Cristina Rodríguez, Antonio Ordóñez, José Martínez-González, Vicente Andrés and Simón Méndez-Ferrer ()
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Raquel del Toro: Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)
Raphael Chèvre: Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)
Cristina Rodríguez: Centro de Investigación Cardiovascular (CSIC-ICCC), IIB-Sant Pau
Antonio Ordóñez: Grupo de Fisiopatología Cardiovascular, Instituto de Biomedicina de Sevilla (IBIS)
José Martínez-González: Centro de Investigación Cardiovascular (CSIC-ICCC), IIB-Sant Pau
Vicente Andrés: Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)
Simón Méndez-Ferrer: Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms12706

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