ArticleCirculation research2013
β-Arrestin-2 deficiency attenuates abdominal aortic aneurysm formation in mice.
Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Elevated levels of neutrophils with a pro-inflammatory profile in Turner syndrome across karyotypes.NPJ genomic medicine · 2025Article
- Nox1/PAK1 is required for angiotensin II-induced vascular inflammation and abdominal aortic aneurysm formation.Redox biology · 2025Article
- Investigation of Strategies to Block Downstream Effectors of AT1R-Mediated Signalling to Prevent Aneurysm Formation in Marfan Syndrome.International journal of molecular sciences · 2024Article
- Insights Into the Role of Angiotensin-II ATHypertension (Dallas, Tex. : 1979) · 2024Review
- DOCK2 Deficiency Attenuates Abdominal Aortic Aneurysm Formation-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Distinct Mechanisms of β-Arrestin-Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality.Hypertension (Dallas, Tex. : 1979) · 2023Article
- ARRB2 (β-Arrestin-2) Deficiency Alters Fluid Homeostasis and Blood Pressure Regulation.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Twenty Years of Studying AngII (Angiotensin II)-Induced Abdominal Aortic Pathologies in Mice: Continuing Questions and Challenges to Provide Insight Into the Human Disease.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Tertiary butylhydroquinone alleviated liver steatosis and increased cell survival via β-arrestin-2/PI3K/AKT pathway.Iranian journal of basic medical sciences · 2021Article
- Self-made allostery: endogenous COMP antagonizes pathologic AT1Cell research · 2021Article
- Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury.Cell research · 2021Article
- Itaconate prevents abdominal aortic aneurysm formation through inhibiting inflammation via activation of Nrf2.EBioMedicine · 2020Article
- Conformational Sensors and Domain Swapping Reveal Structural and Functional Differences between β-Arrestin Isoforms.Cell reports · 2019Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Deficiency of FAM3D (Family With Sequence Similarity 3, Member D), A Novel Chemokine, Attenuates Neutrophil Recruitment and Ameliorates Abdominal Aortic Aneurysm Development.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Astragaloside IV Attenuated 3,4-Benzopyrene-Induced Abdominal Aortic Aneurysm by Ameliorating Macrophage-Mediated Inflammation.Frontiers in pharmacology · 2018Article
- G Protein-Coupled Receptor Signaling Through β-Arrestin-Dependent Mechanisms.Journal of cardiovascular pharmacology · 2017Review
- Molecular pathogenesis of genetic and sporadic aortic aneurysms and dissections.Current problems in surgery · 2017Review
- Calorie restriction protects against experimental abdominal aortic aneurysms in mice.The Journal of experimental medicine · 2016Article
- Background differences in baseline and stimulated MMP levels influence abdominal aortic aneurysm susceptibility.Atherosclerosis · 2015Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAbdominal aortic aneurysms (AAAs) are a chronic inflammatory vascular disease for which pharmacological treatments are not available. A mouse model of AAA formation involves chronic infusion of angiotensin II (AngII), and previous studies indicated a primary role for the AngII type 1a receptor in AAA formation. β-arrestin (βarr)-2 is a multifunctional scaffolding protein that binds G-protein-coupled receptors such as AngII type 1a and regulates numerous signaling pathways and pathophysiological processes. However, a role for βarr2 in AngII-induced AAA formation is currently unknown.
objectiveTo determine whether βarr2 played a role in AngII-induced AAA formation in mice. METHODS AND
resultsTreatment of βarr2(+/+) and βarr2(-/-) mice on the hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) background or on normolipidemic C57BL/6 background with AngII for 28 days indicated that βarr2 deficiency significantly attenuated AAA formation. βarr2 deficiency attenuated AngII-induced expression of cyclooxygenase-2, monocyte chemoattractant protein-1, macrophage inflammatory protein 1α, and macrophage infiltration. AngII also increased the levels of phosphorylated extracellular signal-regulated kinase 1/2 in apoE(-/-)/βarr2(+/+) aortas, whereas βarr2 deficiency diminished this increase. Furthermore, inhibition of extracellular signal-regulated kinase 1/2 activation with CI1040 (100 mg/kg per day) reduced the level of AngII-induced cyclooxygenase-2 expression in apoE(-/-)/βarr2(+/+) mice to the level observed in apoE(-/-)/βarr2(-/-) mice. AngII treatment also increased matrix metalloproteinase expression and disruption of the elastic layer in apoE(-/-)/βarr2(+/+) aortas, and βarr2 deficiency reduced these effects.
conclusionsβarr2 contributes to AngII-induced AAA formation in mice by phosphorylated extracellular signal-regulated kinase 1/2-mediated cyclooxygenase-2 induction and increased inflammation. These studies suggest that for the AngII type 1a receptor, G-protein-independent, βarr2-dependent signaling plays a major role in AngII-induced AAA formation.
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