ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Alternative splicing impairs soluble guanylyl cyclase function in aortic aneurysm.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Challenging the Norm: The Unrecognized Impact of Soluble Guanylyl Cyclase Subunits in Cancer.International journal of molecular sciences · 2024Review
- The perspective of cAMP/cGMP signaling and cyclic nucleotide phosphodiesterases in aortic aneurysm and dissection.Vascular pharmacology · 2024Review
- Per-ARNT-Sim Domains in Nitric Oxide Signaling by Soluble Guanylyl Cyclase.Journal of molecular biology · 2024Review
- Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm.International journal of molecular sciences · 2024Review
- Profiling of the full-length transcriptome in abdominal aortic aneurysm using nanopore-based direct RNA sequencing.Open biology · 2022Article
- Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet-fed rabbits.Pharmacology research & perspectives · 2021Article
- Higher susceptibility to heme oxidation and lower protein stability of the rare αBiochemical pharmacology · 2021Article
- Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their RegulationPhysiological reviews · 2019Review
- The emerging role of alternative splicing in senescence and aging.Aging cell · 2017Review
- Structure and Activation of Soluble Guanylyl Cyclase, the Nitric Oxide Sensor.Antioxidants & redox signaling · 2017Review
- The Role of Reactive Oxygen and Nitrogen Species in the Expression and Splicing of Nitric Oxide Receptor.Antioxidants & redox signaling · 2017Review
- Disrupted nitric oxide signaling due to GUCY1A3 mutations increases risk for moyamoya disease, achalasia and hypertension.Clinical genetics · 2016Article
- The fibrate gemfibrozil is a NO- and haem-independent activator of soluble guanylyl cyclase: in vitro studies.British journal of pharmacology · 2015Article
- Role of sGC-dependent NO signalling and myocardial infarction risk.Journal of molecular medicine (Berlin, Germany) · 2015Review
- Maturation, inactivation, and recovery mechanisms of soluble guanylyl cyclase.The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) receptor soluble guanylyl cyclase (sGC) is a key regulator of several important vascular functions and is important for maintaining cardiovascular homeostasis and vascular plasticity. Diminished sGC expression and function contributes to pathogenesis of several cardiovascular diseases. However, the processes that control sGC expression in vascular tissue remain poorly understood. Previous work in animal and cell models revealed the complexity of alternative splicing of sGC genes and demonstrated its importance in modulation of sGC function. The aim of this study was to examine the role of alternative splicing of α1 and β1 sGC in healthy and diseased human vascular tissue. Our study found a variety of α1 and β1 sGC splice forms expressed in human aorta. Their composition and abundance were different between samples of aortic tissue removed during surgical repair of aortic aneurysm and samples of aortas without aneurysm. Aortas with aneurysm demonstrated decreased sGC activity, which correlated with increased expression of dysfunctional sGC splice variants. In addition, the expression of 55-kDa oxidation-resistant α1 isoform B sGC (α1-IsoB) was significantly lower in aortic samples with aneurysm. The α1-IsoB splice variant was demonstrated to support sGC activity in aortic lysates. Together, our results suggest that alternative splicing contributes to diminished sGC function in vascular dysfunction. Precise understanding of sGC splicing regulation could help to design new therapeutic interventions and to personalize sGC-targeting therapies in treatments of vascular disease.
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