A model of painful vaso-occlusive crisis in mice with sickle cell disease-Reference-Cited by-同舟云学术

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

Published:2022-10-20 Issue:16 Volume:140 Page:1826-1830
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Khasabova Iryna I.¹^ORCID,Juliette Joseph¹^ORCID,Rogness Victoria M.¹^ORCID,Khasabov Sergey G.¹,Golovko Mikhail Y.²^ORCID,Golovko Svetlana A.²,Kiven Stacy³^ORCID,Gupta Kalpna³⁴^ORCID,Belcher John D.⁴^ORCID,Vercellotti Gregory M.⁴,Seybold Virginia S.⁵,Simone Donald A.¹

Affiliation:

1. 1Department of Diagnostic and Biological Sciences, University of Minnesota, Minneapolis, MN

2. 2Department of Biomedical Sciences, University of North Dakota, Grand Forks, ND

3. 3Division of Hematology/Oncology, Department of Medicine, University of California, Irvine, CA

4. 4Division of Hematology, Oncology and Transplantation, Department of Medicine and Vascular Biology Center, University of Minnesota, Minneapolis, MN

5. 5Department of Neuroscience, University of Minnesota, Minneapolis, MN

Abstract

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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

https://ashpublications.org/blood/article-pdf/140/16/1826/1927461/blood_bld-2022-017309-main.pdf

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