ArticleFrontiers in physiology2010
Modification of proteins by norepinephrine is important for vascular contraction.
Article in Frontiers in physiology, 2010. 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, 22 citations in OpenAlex.
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- Inflammation, Autoimmunity, and Hypertension: The Essential Role of Tissue Transglutaminase.American journal of hypertension · 2017Review
- Reduced Noradrenergic Signaling in the Spleen Capsule in the Absence of CBJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Transglutaminase regulation of cell function.Physiological reviews · 2014Review
- The obligatory role of the actin cytoskeleton on inward remodeling induced by dithiothreitol activation of endogenous transglutaminase in isolated arterioles.American journal of physiology. Heart and circulatory physiology · 2014Article
- Transglutaminase 2 promotes PDGF-mediated activation of PDGFR/Akt1 and β-catenin signaling in vascular smooth muscle cells and supports neointima formation.Journal of vascular research · 2014Article
- Bioactivation of the cancer chemopreventive agent tamoxifen to quinone methides by cytochrome P4502B6 and identification of the modified residue on the apoprotein.Drug metabolism and disposition: the biological fate of chemicals · 2012Article
- Histaminylation of glutamine residues is a novel posttranslational modification implicated in G-protein signaling.FEBS letters · 2012Article
- Vena cava and aortic smooth muscle cells express transglutaminases 1 and 4 in addition to transglutaminase 2.American journal of physiology. Heart and circulatory physiology · 2012Article
- Cellular functions of tissue transglutaminase.International review of cell and molecular biology · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Norepinephrine (NE) is thought to mediate its effects through G-protein coupled receptors. However, previous studies have shown that NE and another primary amine, serotonin, also have the ability to exert effects in a receptor-independent manner. We hypothesized that the enzyme transglutaminase II (TG II) has the ability to modify proteins with NE and that this modification is physiologically relevant. As our model we used rat aortic and vena cava tissues, two tissues that depend on NE to modulate vascular tone. Immunohistochemical and immunocytochemical staining showed that NE and TG II are present in smooth muscle cells of these tissues. Western analysis shows aorta and vena cava homogenate proteins are recognized by an antibody raised against NE conjugated to bovine serum albumin (NE-BSA). NE and α-actin colocalize in cultured aorta and vena cava smooth muscle cells. Freshly dissociated smooth muscle cells from these vessels were able to take up NE-biotin. In isolated tissue baths, inhibition of TG II with cystamine (0.5 mM) completely abolished NE-induced contraction in the aorta but only attenuated the receptor-independent contractant KCl (max contraction to 100 mM KCl in cystamine treated = 88.8 ± 7.0% of vehicle treated, p < 0.05). In the vena cava, contraction to NE was abolished with 0.1 mM cystamine and KCl contraction was attenuated (max contraction to 100 mM KCl in cystamine treated = 54.8 ± 7.0% of vehicle treated, p < 0.05). Taken together, these results show that vascular smooth muscle cells take up and utilize NE for the modification of proteins, and that this modification may play an important role in vascular contraction.
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