ArticleThe journal of sexual medicine2010
p38 Mitogen-activated protein kinase (MAPK) increases arginase activity and contributes to endothelial dysfunction in corpora cavernosa from angiotensin-II-treated mice.
Article in The journal of sexual medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Pathophysiology of Arginases in Cancer and Efforts in Their Pharmacological Inhibition.International journal of molecular sciences · 2024Review
- Downregulation of the expression of galanin impairs erectile function in hypoandrogenic rats.Sexual medicine · 2023Article
- Methylglyoxal-Modified Albumin Effects on Endothelial Arginase Enzyme and Vascular Function.Cells · 2023Article
- Hyperglycemia-impaired aortic vasorelaxation mediated through arginase elevation: Role of stress kinase pathways.European journal of pharmacology · 2019Article
- Influence of arginase polymorphisms and arginase levels/activity on the response to erectile dysfunction therapy with sildenafil.The pharmacogenomics journal · 2018Article
- PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway.Scientific reports · 2017Article
- Glucocorticoids improve endothelial function in rheumatoid arthritis: a study in rats with adjuvant-induced arthritis.Clinical and experimental immunology · 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 II limits NO production by upregulating arginase through a p38 MAPK-ATF-2 pathway.European journal of pharmacology · 2015Article
- Article
- Angiotensin II-induced arterial thickening, fibrosis and stiffening involves elevated arginase function.PloS one · 2015Article
- Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function.Journal of hematology & oncology · 2014Review
- p38 mitogen-activated protein kinase is involved in arginase-II-mediated eNOS-uncoupling in obesity.Cardiovascular diabetology · 2014Article
- Functions of arginase isoforms in macrophage inflammatory responses: impact on cardiovascular diseases and metabolic disorders.Frontiers in immunology · 2014Review
- Activated Rho kinase mediates diabetes-induced elevation of vascular arginase activation and contributes to impaired corpora cavernosa relaxation: possible involvement of p38 MAPK activation.The journal of sexual medicine · 2013Article
- Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.Cardiovascular research · 2013Article
- Selenium inhibits renal oxidation and inflammation but not acute kidney injury in an animal model of rhabdomyolysis.Antioxidants & redox signaling · 2013Article
- Akita spontaneously type 1 diabetic mice exhibit elevated vascular arginase and impaired vascular endothelial and nitrergic function.PloS one · 2013Article
- Vasomotor regulation of coronary microcirculation by oxidative stress: role of arginase.Frontiers in immunology · 2013Article
- Arginase 1 mediates increased blood pressure and contributes to vascular endothelial dysfunction in deoxycorticosterone acetate-salt hypertension.Frontiers in immunology · 2013Article
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10 authors at 1 institution in 1 country.
Funding
Abstract
introductionAngiotensin II (AngII) activates p38 mitogen-activated protein kinase (MAPK) and elevates arginase activity in endothelial cells. Upregulation of arginase activity has been implicated in endothelial dysfunction by reducing nitric oxide (NO) bioavailability. However, signaling pathways activated by AngII in the penis are largely unknown.
aimWe hypothesized that activation of p38 MAPK increases arginase activity and thus impairs penile vascular function in AngII-treated mice.
methodsMale C57BL/6 mice were implanted with osmotic minipumps containing saline or AngII (42 µg/kg/h) for 14 days and cotreated with p38 MAPK inhibitor, SB 203580 (5 µg/kg/day), beginning 2 days before minipump implantation. Systolic blood pressure (SBP) was measured. Corpus cavernosum (CC) tissue was used for vascular functional studies and protein expression levels of p38 MAPK, arginase and constitutive NO synthase (NOS), and arginase activity.
main outcome measuresArginase expression and activity; expression of phospho-p38 MAPK, endothelial NOS (eNOS) and neuronal NOS proteins; endothelium-dependent and nitrergic nerve-mediated relaxations were determined in CC from control and AngII-infused mice.
resultsAngII increased SBP (22%) and increased CC arginase activity and expression (∼twofold), and phosphorylated P38 MAPK levels (30%) over control. Treatment with SB 203580 prevented these effects. Endothelium-dependent NO-mediated relaxation to acetylcholine was significantly reduced by AngII and this effect was prevented by SB 203580 (P < 0.01). AngII (2 weeks) did not alter nitrergic function. However, SB 203580 significantly increased nitrergic relaxation in both control and AngII tissue at lower frequencies. Maximum contractile responses for phenylephrine and electrical field stimulation were increased by AngII (56% and 171%, respectively) and attenuated by SB 203580 treatment. AngII treatment also decreased eNOS phosphorylation at Ser-1177 compared to control. Treatment with SB 203580 prevented all these changes.
conclusionp38 MAPK inhibition corrects penile arginase activity and protects against erectile dysfunction caused by AngII.
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