ArticleAmerican journal of physiology. Cell physiology2010
Thrombin induces endothelial arginase through AP-1 activation.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Targeting Arginine in COVID-19-Induced Immunopathology and Vasculopathy.Metabolites · 2022Review
- Acacetin improves endothelial dysfunction and aortic fibrosis in insulin-resistant SHR rats by estrogen receptors.Molecular biology reports · 2020Article
- Requisite roles of LOX-1, JNK, and arginase in diabetes-induced endothelial vasodilator dysfunction of porcine coronary arterioles.Journal of molecular and cellular cardiology · 2019Article
- Altered Cd8+ T lymphocyte Response Triggered by Arginase 1: Implication for Fatigue Intensification during Localized Radiation Therapy in Prostate Cancer Patients.Neuropsychiatry · 2018Article
- The Arginase Pathway in Neonatal Brain Hypoxia-Ischemia.Developmental neuroscience · 2018Review
- Arginase Inhibition Reverses Monocrotaline-Induced Pulmonary Hypertension.International journal of molecular sciences · 2017Article
- Article
- Coagulation induced by C3aR-dependent NETosis drives protumorigenic neutrophils during small intestinal tumorigenesis.Nature communications · 2016Article
- Tissue-specific up-regulation of arginase I and II induced by p38 MAPK mediates endothelial dysfunction in type 1 diabetes mellitus.British journal of pharmacology · 2015Article
- Angiotensin II limits NO production by upregulating arginase through a p38 MAPK-ATF-2 pathway.European journal of pharmacology · 2015Article
- Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart.Frontiers in physiology · 2015Review
- cAMP-responsive element-binding protein (CREB) and cAMP co-regulate activator protein 1 (AP1)-dependent regeneration-associated gene expression and neurite growth.The Journal of biological chemistry · 2014Article
- Functions of arginase isoforms in macrophage inflammatory responses: impact on cardiovascular diseases and metabolic disorders.Frontiers in immunology · 2014Review
- Role of arginase in vessel wall remodeling.Frontiers in immunology · 2013Article
- Arginase: the emerging therapeutic target for vascular oxidative stress and inflammation.Frontiers in immunology · 2013Article
- ATF2 - at the crossroad of nuclear and cytosolic functions.Journal of cell science · 2012Article
- Regulation of macrophage arginase expression and tumor growth by the Ron receptor tyrosine kinase.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- High glucose-treated macrophages augment E-selectin expression in endothelial cells.The Journal of biological chemistry · 2011Article
- Angiotensin II-induced vascular endothelial dysfunction through RhoA/Rho kinase/p38 mitogen-activated protein kinase/arginase pathway.American journal of physiology. Cell physiology · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Arterial thrombosis is a common disease leading to severe ischemia beyond the obstructing thrombus. Additionally, endothelial dysfunction at the site of thrombosis can be rescued by l-arginine supplementation or arginase blockade in several animal models. Exposure of rat aortic endothelial cells (RAECs) to thrombin upregulates arginase I mRNA and protein levels. In this study, we further investigated the molecular mechanism of thrombin-induced arginase changes in endothelial cells. Thrombin strikingly increased arginase I promoter and enzyme activity in primary cultured RAECs. Using different deletion and point mutations of the promoter, we demonstrated that the activating protein-1 (AP-1) consensus site located at -3,157 bp in the arginase I promoter was a thrombin-responsive element. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay further confirmed that upon thrombin stimulation, c-Jun and activating transcription factor-2 (ATF-2) bound to the AP-1 site, which initiated the transactivation. Moreover, loss-of-function studies using small interfering RNA confirmed that recruitment of these two transcription factors to the AP-1 site was required for thrombin-induced arginase upregulation. In the course of defining the signaling pathway leading to the activation of AP-1 by thrombin, we found thrombin-induced phosphorylation of stress-activated protein kinase/c-Jun-NH(2)-terminal kinase (SAPK/JNK or JNK1/2/3) and p38 mitogen-activated protein kinase, which were followed by the phosphorylation of both c-Jun and ATF-2. These findings reveal the basis for thrombin induction of endothelial arginase I and indicate that arginase inhibition may be an attractive therapeutic alternative in the setting of arterial thrombosis and its associated endothelial dysfunction.
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