ArticleCommunicative & integrative biology2011
Nitric oxide regulates non-classical secretion of tissue transglutaminase.
Article in Communicative & integrative biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- An mTORC1-GRASP55 signaling axis controls unconventional secretion to reshape the extracellular proteome upon stress.Molecular cell · 2021Article
- Spotlight on the Transglutaminase 2-Heparan Sulfate Interaction.Medical sciences (Basel, Switzerland) · 2019Review
- Transglutaminases in Monocytes and Macrophages.Medical sciences (Basel, Switzerland) · 2018Review
- Endothelial cell-surface tissue transglutaminase inhibits neutrophil adhesion by binding and releasing nitric oxide.Scientific reports · 2017Article
- Tissue Transglutaminase Modulates Vascular Stiffness and Function Through Crosslinking-Dependent and Crosslinking-Independent Functions.Journal of the American Heart Association · 2017Article
- Shock Wave Enhances Angiogenesis through VEGFR2 Activation and Recycling.Molecular medicine (Cambridge, Mass.) · 2017Article
- Characterization of distinct sub-cellular location of transglutaminase type II: changes in intracellular distribution in physiological and pathological states.Cell and tissue research · 2014Article
- Exercise, vascular stiffness, and tissue transglutaminase.Journal of the American Heart Association · 2014Article
- Transglutaminase 2-mediated serotonylation in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Increased tissue transglutaminase activity contributes to central vascular stiffness in eNOS knockout mice.American journal of physiology. Heart and circulatory physiology · 2013Article
- Nonclassically Secreted Regulators of Angiogenesis.Angiology: open access · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) is an endogenous second messenger which acts as a potent vasodilator, anti-inflammatory, anti-thrombotic and pro-angiogenic agent in the vasculature. Recent studies revealed that the effects of NO on blood vessels are mediated in part by its ability to regulate protein trafficking machinery and vesicle-based exocytosis in vascular cells. Specifically, NO-dependent S-nitrosylation of N-ethylmaleimide sensitive factor (NSF), an ATPase that enables membrane fusion, was shown to inhibit exocytosis of vesicular secretory compartments such as endothelial Weibel-Palade bodies, platelet alpha granules and cytolytic granules from activated lymphocytes. Tissue transglutaminase (tTG or TG2) is a multifunctional protein synthesized and secreted by various cell types in the vasculature, which is involved in multiple vascular diseases, including atherosclerosis, vascular calcification and age-dependent aortic stiffening. Our recent findings indicate that tTG is delivered to the cell surface and the extracellular matrix (ECM) via a non-classical ER/Golgi-independent secretion pathway, which depends on the recycling endosomes and the NSF function. Here we report that NO attenuates the unconventional secretion of tTG in human aortic endothelial cells. NO-dependent downregulation of extracellular tTG levels via inhibition of its secretion might be a part of general physiological mechanism which limits externalization of adhesive, pro-inflammatory and thrombogenic proteins in the vasculature.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.