ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Increased tissue transglutaminase activity contributes to central vascular stiffness in eNOS knockout mice.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- Biomarker advancements in cerebral small vessel disease: An overview.Neural regeneration research · 2026Article
- LOXL2 inhibition ameliorates pulmonary artery remodeling in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Sex differences and role of lysyl oxidase-like 2 in angiotensin II-induced hypertension in mice.American journal of physiology. Heart and circulatory physiology · 2024Article
- Adenosine AJournal of the American Heart Association · 2023Article
- S-Nitrosylation of Tissue Transglutaminase in Modulating Glycolysis, Oxidative Stress, and Inflammatory Responses in Normal and Indoxyl-Sulfate-Induced Endothelial Cells.International journal of molecular sciences · 2023Article
- BACE1: More than just a β-secretase.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022Review
- Vascular Stiffening Mediated by Rho-Associated Coiled-Coil Containing Kinase Isoforms.Journal of the American Heart Association · 2021Article
- Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix.International journal of molecular sciences · 2021Review
- Gut Microbiome-Derived Metabolite Trimethylamine N-Oxide Induces Aortic Stiffening and Increases Systolic Blood Pressure With Aging in Mice and Humans.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Probing tissue transglutaminase mediated vascular smooth muscle cell aging using a novel transamidation-deficient Tgm2-C277S mouse model.Cell death discovery · 2021Article
- Deficiency of Endothelial Nitric Oxide Synthase (eNOS) Exacerbates Brain Damage and Cognitive Deficit in A Mouse Model of Vascular Dementia.Aging and disease · 2021Article
- The Progress of Advanced Ultrasonography in Assessing Aortic Stiffness and the Application Discrepancy between Humans and Rodents.Diagnostics (Basel, Switzerland) · 2021Review
- Mechanobiology of Microvascular Function and Structure in Health and Disease: Focus on the Coronary Circulation.Frontiers in physiology · 2021Review
- Vascular function is further impaired in subjects aged 80 years or older.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Restoring Blood Pressure in Hypertensive Mice Fails to Fully Reverse Vascular Stiffness.Frontiers in physiology · 2020Article
- Deletion of the microRNA-degrading nuclease, translin/trax, prevents pathogenic vascular stiffness.American journal of physiology. Heart and circulatory physiology · 2019Article
- Age-Dependent Impairment in Endothelial Function and Arterial Stiffness in Former High Class Male Athletes Is No Different to That in Men With No History of Physical Training.Journal of the American Heart Association · 2019Article
- Arterial Stiffness Assessed by Cardio-Ankle Vascular Index.International journal of molecular sciences · 2019Review
- Lysyl oxidase-like 2 depletion is protective in age-associated vascular stiffening.American journal of physiology. Heart and circulatory physiology · 2019Article
- Regenerative and durable small-diameter graft as an arterial conduit.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Nitric oxide (NO) can modulate arterial stiffness by regulating both functional and structural changes in the arterial wall. Tissue transglutaminase (TG2) has been shown to contribute to increased central aortic stiffness by catalyzing the cross-linking of matrix proteins. NO S-nitrosylates and constrains TG2 to the cytosolic compartment and thereby holds its cross-linking function latent. In the present study, the role of endothelial NO synthase (eNOS)-derived NO in regulating TG2 function was studied using eNOS knockout mice. Matrix-associated TG2 and TG2 cross-linking function were higher, whereas TG2 S-nitrosylation was lower in the eNOS(-/-) compared with wild-type (WT) mice. Pulse-wave velocity (PWV) and blood pressure measured noninvasively were elevated in the eNOS(-/-) compared with WT mice. Intact aortas and decellularized aortic tissue scaffolds of eNOS(-/-) mice were significantly stiffer, as determined by tensile testing. The carotid arteries of the eNOS(-/-) mice were also stiffer, as determined by pressure-dimension analysis. Invasive methods to determine the PWV-mean arterial pressure relationship showed that PWV in eNOS(-/-) and WT diverge at higher mean arterial pressure. Thus eNOS-derived NO regulates TG2 localization and function and contributes to vascular stiffness.
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