Autor: |
Peter Libby, Vanessa Frodermann, Friedrich Felix Hoyer, Christoph J. Binder, Christopher T. Chan, Annemijn F. Gregory, Yoshiko Iwamoto, Anne Vassalli, Cameron S. McAlpine, Matthias Nahrendorf, Atsushi Anzai, Filip K. Swirski, Thomas E. Scammell, Shun He, Florian Kahles, Wolfram C. Poller, Ashley M. Fenn, Mehdi Tafti, John E. Mindur, Colin Valet, Sara Rattik, Lennard Halle, M. Kiss |
Jazyk: |
angličtina |
Rok vydání: |
2019 |
Předmět: |
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Zdroj: |
Nature Nature, vol. 566, no. 7744, pp. 383-387 |
ISSN: |
1476-4687 0028-0836 |
Popis: |
Sleep is integral to life 1 . Although insufficient or disrupted sleep increases the risk of multiple pathological conditions, including cardiovascular disease 2 , 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-6C high 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. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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