Sleep modulates haematopoiesis and protects against atherosclerosis

Cameron S. McAlpine, Máté G. Kiss, Sara Rattik, Shun He, Anne Vassalli, Colin Valet, Atsushi Anzai, Christopher T. Chan, John E. Mindur, Florian Kahles, Wolfram C. Poller, Vanessa Frodermann, Ashley M. Fenn, Annemijn F. Gregory, Lennard Halle, Yoshiko Iwamoto, Friedrich F. Hoyer, Christoph J. Binder, Peter Libby, Mehdi TaftiThomas E. Scammell, Matthias Nahrendorf, Filip K. Swirski

研究成果: Article査読

226 被引用数 (Scopus)


Sleep is integral to life1. Although insufficient or disrupted sleep increases the risk of multiple pathological conditions, including cardiovascular disease2, we know little about the cellular and molecular mechanisms by which sleep maintains cardiovascular health. Here we report that sleep regulates haematopoiesis and protects against atherosclerosis in mice. We show that mice subjected to sleep fragmentation produce more Ly-6Chigh monocytes, develop larger atherosclerotic lesions and produce less hypocretin—a stimulatory and wake-promoting neuropeptide—in the lateral hypothalamus. Hypocretin controls myelopoiesis by restricting the production of CSF1 by hypocretin-receptor-expressing pre-neutrophils in the bone marrow. Whereas hypocretin-null and haematopoietic hypocretin-receptor-null mice develop monocytosis and accelerated atherosclerosis, sleep-fragmented mice with either haematopoietic CSF1 deficiency or hypocretin supplementation have reduced numbers of circulating monocytes and smaller atherosclerotic lesions. Together, these results identify a neuro-immune axis that links sleep to haematopoiesis and atherosclerosis.

出版ステータスPublished - 2019 2月 21

ASJC Scopus subject areas

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