Hyperlipidemia does not affect development of elastase-induced abdominal aortic aneurysm in mice.
Abdominal aortic aneurysm
Animal model
Hyperlipidemia
Pathobiology
Journal
Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
18
05
2020
revised:
31
07
2020
accepted:
26
08
2020
pubmed:
20
9
2020
medline:
24
6
2021
entrez:
19
9
2020
Statut:
ppublish
Résumé
Hyperlipidemia is a suggested risk factor for abdominal aortic aneurysm (AAA). However, whether hyperlipidemia is causally involved in AAA progression remains elusive. Here, we tested the hypothesis that hyperlipidemia aggravates AAA formation in the widely used porcine pancreatic elastase (PPE) model of AAA in mice with varying levels of plasma lipids. Prior to PPE-surgery, 8-week-old male C57BL/6J mice (n = 32) received 1·10 At sacrifice, maximal intergroup plasma cholesterol and non-HDL/HDL ratio differences were >5-fold and >20-fold, respectively. AAA diameters expanded to 150% of baseline, but no intergroup differences were detected. This was verified in an independent experiment comparing 8-week-old male ApoE In summary, we find that lipid deposition in the aortic wall is a feature of PPE-induced AAA in mice as well as human AAA lesions. Despite, our data do not support the hypothesis that hyperlipidemia contributes to AAA progression.
Sections du résumé
BACKGROUND AND AIMS
Hyperlipidemia is a suggested risk factor for abdominal aortic aneurysm (AAA). However, whether hyperlipidemia is causally involved in AAA progression remains elusive. Here, we tested the hypothesis that hyperlipidemia aggravates AAA formation in the widely used porcine pancreatic elastase (PPE) model of AAA in mice with varying levels of plasma lipids.
METHODS
Prior to PPE-surgery, 8-week-old male C57BL/6J mice (n = 32) received 1·10
RESULTS
At sacrifice, maximal intergroup plasma cholesterol and non-HDL/HDL ratio differences were >5-fold and >20-fold, respectively. AAA diameters expanded to 150% of baseline, but no intergroup differences were detected. This was verified in an independent experiment comparing 8-week-old male ApoE
CONCLUSIONS
In summary, we find that lipid deposition in the aortic wall is a feature of PPE-induced AAA in mice as well as human AAA lesions. Despite, our data do not support the hypothesis that hyperlipidemia contributes to AAA progression.
Identifiants
pubmed: 32949946
pii: S0021-9150(20)30456-1
doi: 10.1016/j.atherosclerosis.2020.08.012
pii:
doi:
Substances chimiques
Pancreatic Elastase
EC 3.4.21.36
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
73-83Subventions
Organisme : NHLBI NIH HHS
ID : R56 HL135654
Pays : United States
Organisme : BLRD VA
ID : I01 BX002641
Pays : United States
Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.