A model of painful vaso-occlusive crisis in mice with sickle cell disease

In order to better understand mechanisms underlying acute pain during vaso-occlusive crises (VOCs) in patients with sickle cell disease, Khasabova et al report on a clinically relevant model in mice where VOC is stimulated by exposure to cold. Cold exposure produces robust hyperalgesia, stasis, hypo...

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Bibliographic Details
Published in:Blood 2022-10, Vol.140 (16), p.1826-1830
Main Authors: Khasabova, Iryna I., Juliette, Joseph, Rogness, Victoria M., Khasabov, Sergey G., Golovko, Mikhail Y., Golovko, Svetlana A., Kiven, Stacy, Gupta, Kalpna, Belcher, John D., Vercellotti, Gregory M., Seybold, Virginia S., Simone, Donald A.
Format: Article
Language:English
Subjects:
Anemia, Sickle Cell - complications
Animals
Hemoglobinopathies
Letter to Blood
Mice
Pain - etiology
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Summary:In order to better understand mechanisms underlying acute pain during vaso-occlusive crises (VOCs) in patients with sickle cell disease, Khasabova et al report on a clinically relevant model in mice where VOC is stimulated by exposure to cold. Cold exposure produces robust hyperalgesia, stasis, hypoxia, elevated heart rate, and increased levels of the endocannabinoid 2-AG and its synthesizing enzyme, DAGLβ, in plasma and blood cells, respectively. Blocking DAGLβ prevents the development of hyperalgesia. Collectively, these data point to 2-AG signaling as a targetable mediator of VOC pain.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.2022017309