ArticleEuropean journal of pharmacology2015
Angiotensin II limits NO production by upregulating arginase through a p38 MAPK-ATF-2 pathway.
Article in European journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Hypertension: Potential Player in Cardiovascular Disease Incidence in Preeclampsia.Cardiovascular toxicology · 2022Review
- Mutation in FBXO32 causes dilated cardiomyopathy through up-regulation of ER-stress mediated apoptosis.Communications biology · 2021Article
- Steroid-Induced Osteonecrosis of the Femoral Head: Novel Insight Into the Roles of Bone Endothelial Cells in Pathogenesis and Treatment.Frontiers in cell and developmental biology · 2021Review
- Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension.Redox biology · 2020Article
- Hyperglycemia-impaired aortic vasorelaxation mediated through arginase elevation: Role of stress kinase pathways.European journal of pharmacology · 2019Article
- Maladaptive aortic remodeling in hypertension associates with dysfunctional smooth muscle contractility.American journal of physiology. Heart and circulatory physiology · 2019Article
- Article
- Nuclear factor-erythroid 2-related factor 3 (NRF3) is low expressed in colorectal cancer and its down-regulation promotes colorectal cancer malignance through activating EGFR and p38/MAPK.American journal of cancer research · 2019Article
- Silencing activating transcription factor 2 promotes the anticancer activity of sorafenib in hepatocellular carcinoma cells.Molecular medicine reports · 2018Article
- Mechanisms of Diabetes-Induced Endothelial Cell Senescence: Role of Arginase 1.International journal of molecular sciences · 2018Article
- Arginase: A Multifaceted Enzyme Important in Health and Disease.Physiological reviews · 2018Review
- EPA:DHA 6:1 prevents angiotensin II-induced hypertension and endothelial dysfunction in rats: role of NADPH oxidase- and COX-derived oxidative stress.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- NOX2-Induced Activation of Arginase and Diabetes-Induced Retinal Endothelial Cell Senescence.Antioxidants (Basel, Switzerland) · 2017Article
- Supplementation with Phycocyanobilin, Citrulline, Taurine, and Supranutritional Doses of Folic Acid and Biotin-Potential for Preventing or Slowing the Progression of Diabetic Complications.Healthcare (Basel, Switzerland) · 2017Article
- Vascular surgical stretch injury leads to activation of P2X7 receptors and impaired endothelial function.PloS one · 2017Article
- 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-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads.Journal of the renin-angiotensin-aldosterone system : JRAASReview
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Enhanced vascular arginase activity can impair endothelium-dependent vasorelaxation by decreasing l-arginine availability to endothelial nitric oxide (NO) synthase, thereby reducing NO production and uncoupling NOS function. Elevated angiotensin II (Ang II) is a key component of endothelial dysfunction in many cardiovascular diseases and has been linked to elevated arginase activity. In this study we explored the signaling pathway leading to increased arginase expression/activity in response to Ang II in bovine aortic endothelial cells (BAEC). Our previous studies indicate involvement of p38 mitogen activated protein kinase (MAPK) in Ang II-induced arginase upregulation and reduced NO production. In this study, we further investigated the Ang II-transcriptional regulation of arginase 1 in endothelial cells. Our results indicate the involvement of ATF-2 transcription factor of the AP1 family in arginase 1 upregulation and in limiting NO production. Using small interfering RNA (siRNA) targeting ATF-2, we showed that this transcription factor is required for Ang II-induced arginase 1 gene upregulation and increased arginase 1 expression and activity, leading to reduced NO production. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay further confirmed the involvement of ATF-2. Moreover, our data indicate that p38 MAPK phosphorylates ATF-2 in response to Ang II. Collectively, our results indicate that Ang II increases endothelial arginase activity/expression through a p38 MAPK/ATF-2 pathway leading to reduced endothelial NO production. These signaling steps might be therapeutic targets for preventing vascular endothelial dysfunction associated with elevated arginase activity/expression.
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