Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Type I interferon receptor subunit 1 deletion attenuates experimental abdominal aortic aneurysm formation

Takahiro Shoji
ORCID logo ,
Jia Guo
,
Yingbin Ge
ORCID logo ,
Yankui Li
,
Gang Li
,
Toru Ikezoe
,
Wei Wang
,
Xiaoya Zheng
,
Sihai Zhao
ORCID logo ,
Naoki Fujimura
,
Jianhua Huang
,
Baohui Xu
* ORCID logo ,
Ronald L. Dalman
*
Version 1 : Received: 15 September 2022 / Approved: 19 September 2022 / Online: 19 September 2022 (02:08:07 CEST)

A peer-reviewed article of this Preprint also exists.

Shoji, T.; Guo, J.; Ge, Y.; Li, Y.; Li, G.; Ikezoe, T.; Wang, W.; Zheng, X.; Zhao, S.; Fujimura, N.; Huang, J.; Xu, B.; Dalman, R.L. Type I Interferon Receptor Subunit 1 Deletion Attenuates Experimental Abdominal Aortic Aneurysm Formation. Biomolecules 2022, 12, 1541. Shoji, T.; Guo, J.; Ge, Y.; Li, Y.; Li, G.; Ikezoe, T.; Wang, W.; Zheng, X.; Zhao, S.; Fujimura, N.; Huang, J.; Xu, B.; Dalman, R.L. Type I Interferon Receptor Subunit 1 Deletion Attenuates Experimental Abdominal Aortic Aneurysm Formation. Biomolecules 2022, 12, 1541.

Abstract

Objective: Type I interferon receptor (IFNAR) signaling contributes to several autoimmune and vascular diseases such as atherosclerosis and stroke. The purpose of this study was to assess the influence of IFNAR1 deficiency on the formation and progression of experimental abdominal aortic aneurysms (AAAs). Methods: AAAs were induced in type I interferon receptor subunit 1 (IFNAR1) deficient and wild type control male mice via intra-infrarenal aortic infusion of porcine pancreatic elastase. Immunostaining for IFNAR1 was evaluated in experimental and clinical aneurysms. The initiation and progression of experimental AAAs was assessed via ultrasound imaging prior to (day 0) and 3-, 7-, and 14-days following elastase infusion. Aneurysmal histopathology was analyzed at sacrifice. Results: Increased aortic medial and adventitial IFNAR1 expression was present in both clinical AAAs harvested at surgery and experimental AAAs. Following AAA initiation, wild type mice experienced progressive, time-dependent infrarenal aortic enlargement. This progression was substantially attenuated in IFNAR1 deficient mice. On histological analyses, medial elastin degradation, smooth muscle cell depletion, leukocyte accumulation and neoangiogenesis were markedly diminished in IFNAR1 deficient as compared to wild type mice. Conclusion: IFNAR1 deficiency limited experimental AAA progression in response to intra-aortic elastase infusion. Combined with clinical observations, these results suggest a regulatory role for IFNAR1 activity in AAA pathogenesis.

Keywords

Abdominal aortic aneurysm; Type I interferon receptor, Leukocytes; Angiogenesis

Subject

Medicine and Pharmacology, Pathology and Pathobiology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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