CD38 deficient mice are not protected from atherosclerosis.

Autor: Kong XY; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway. Electronic address: x.y.kong@medisin.uio.no., Lauritzen KH; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway., Dahl TB; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway., Holm S; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway., Olsen MB; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway., Skjelland M; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Oslo, Norway., Nielsen C; Department of Chronic Diseases, Norwegian Institute of Public Health, Oslo, Norway; Department of Pain Management and Research, Oslo University Hospital, Oslo, Norway., Michelsen AE; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway., Ueland T; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Thrombosis Research Center (TREC), Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway., Aukrust P; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway., Halvorsen B; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway., Sandanger Ø; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Section of Dermatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Apr 23; Vol. 705, pp. 149734. Date of Electronic Publication: 2024 Feb 27.
DOI: 10.1016/j.bbrc.2024.149734
Abstrakt: CD38 is a multifunctional enzyme implicated in chemotaxis of myeloid cells and lymphocyte activation, but also expressed by resident cells such as endothelial and smooth muscle cells. CD38 is important for host defense against microbes. However, CD38's role in the pathogenesis of atherosclerosis is controversial with seemingly conflicting results reported so far. To clarify the discrepancy of current literature on the effect of CD38 ablation on atherosclerosis development, we implanted a shear stress modifier around the right carotid artery in CD38 -/- and WT mice. Hypercholesterolemia was induced by human gain-of-function PCSK9 (D374Y), introduced using AAV vector (serotype 9), combined with an atherogenic diet for a total of 9 weeks. Atherosclerosis was assessed at the aortic root, aortic arch and the right carotid artery. The findings can be summarized as follows: i) CD38 -/- and WT mice had a similar atherosclerotic burden in all three locations, ii) No significant differences in monocyte infiltration or macrophage content could be seen in the plaques, and iii) The amount of collagen deposition in the plaques were also similar between CD38 -/- and WT mice. In conclusion, our data suggest that CD38 -/- mice are neither protected against nor prone to atherosclerosis compared to WT mice.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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