ArticleAmerican journal of physiology. Heart and circulatory physiology2015
The role of β-arrestin2-dependent signaling in thoracic aortic aneurysm formation in a murine model of Marfan syndrome.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Characterization of genetic variants of GIPR reveals a contribution of β-arrestin to metabolic phenotypes.Nature metabolism · 2024Article
- 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
- 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
- [Naringenin inhibits thoracic aortic aneurysm formation in mice with Marfan syndrome].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022Article
- Marfan syndrome.Nature reviews. Disease primers · 2021Review
- Transforming Growth Factor β Receptor Type I Inhibitor, Galunisertib, Has No Beneficial Effects on Aneurysmal Pathological Changes in Marfan Mice.Biomolecules & therapeutics · 2020Article
- Marfan syndrome; A connective tissue disease at the crossroads of mechanotransduction, TGFβ signaling and cell stemness.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- TGF-β Signaling-Related Genes and Thoracic Aortic Aneurysms and Dissections.International journal of molecular sciences · 2018Review
- 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
- Vascular smooth muscle cells in Marfan syndrome aneurysm: the broken bricks in the aortic wall.Cellular and molecular life sciences : CMLS · 2017Review
- Smooth muscle cell-specific Tgfbr1 deficiency promotes aortic aneurysm formation by stimulating multiple signaling events.Scientific reports · 2016Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Ang II type 1a receptor (AT1aR)-mediated activation of MAPKs contributes to thoracic aortic aneurysm (TAA) development in Marfan syndrome (MFS). β-Arrestin2 (βarr2) is known to mediate AT1aR-dependent MAPK activation, as well as proproliferative and profibrotic signaling in aortic vascular smooth muscle cells. Therefore, we investigated whether βarr2-dependent signaling contributes to TAA formation in MFS. We used a murine model of MFS [fibrillin (Fbn)(C1039G/+)] to generate an MFS murine model in combination with genetic βarr2 deletion (Fbn(C1039G/+)/βarr2(-/-)). Fbn(C1039G/+)/βarr2(-/-) mice displayed delayed aortic root dilation compared with Fbn(C1039G/+) mice. The mRNA and protein expression of several mediators of TAA formation, including matrix metalloproteinase (MMP)-2 and -9, was reduced in the aorta of Fbn(C1039G/+)/βarr2(-/-) mice relative to Fbn(C1039G/+) mice. Activation of ERK1/2 was also decreased in the aortas of Fbn(C1039G/+)/βarr2(-/-) mice compared with Fbn(C1039G/+) animals. Small interfering RNA targeting βarr2 inhibited angiotensin-stimulated expression of proaneurysmal signaling mediators in primary aortic root smooth muscle cells. Angiotensin-stimulated expression of the proaneurysmal signaling mediators MMP-2 and -9 was inhibited by blockade of ERK1/2 or the EGF receptor, whereas blockade of the transforming growth factor-β receptor had no effect. These results suggest that βarr2 contributes to TAA formation in MFS by regulating ERK1/2-dependent expression of proaneurysmal genes and proteins downstream of the AT1aR. Importantly, this demonstration of the unique signaling mechanism by which βarr2 contributes to aneurysm formation identifies multiple novel, potential therapeutic targets in MFS.
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