ArticleEndocrinology2009
Endothelial dysfunction in mice with streptozotocin-induced type 1 diabetes is opposed by compensatory overexpression of cyclooxygenase-2 in the vasculature.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 72 citations in OpenAlex.
- PARP-1 inhibition attenuates tumor pathology in a novel murine model of diabetes-associated colitis-induced colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Small things matter: Lack of extraislet β cells in type 1 diabetes.Science advances · 2025Article
- Endothelial function can be modulated by acute hyperglycemia.Scientific reports · 2025Article
- Glyoxalase-1 overexpression attenuates arterial wall stiffening in diabetic mice.Cardiovascular diabetology · 2025Article
- Long-Term Effects of Suramin on Renal Function in Streptozotocin-Induced Diabetes in Rats.International journal of molecular sciences · 2023Article
- The effects of oralHeliyon · 2021Article
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- α-Ketoglutarate Upregulates Collecting Duct (Pro)renin Receptor Expression, Tubular Angiotensin II Formation, and NaFrontiers in cardiovascular medicine · 2021Article
- Elevated circulating amyloid concentrations in obesity and diabetes promote vascular dysfunction.The Journal of clinical investigation · 2020Article
- Functional changes in vascular reactivity to adenosine receptor activation in type I diabetic mice.European journal of pharmacology · 2018Article
- Article
- Rho-kinase and the nitric oxide pathway modulate basilar arterial reactivity to acetylcholine and angiotensin II in streptozotocin-induced diabetic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Small protein A and phospholipase D immunization serves a protective role in a mouse pneumonia model of Acinetobacter baumannii infection.Molecular medicine reports · 2017Article
- Celecoxib Alleviates Memory Deficits by Downregulation of COX-2 Expression and Upregulation of the BDNF-TrkB Signaling Pathway in a Diabetic Rat Model.Journal of molecular neuroscience : MN · 2017Article
- Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes.Scientific reports · 2017Article
- Article
- Inhibition of cyclooxygenase-2 causes a decrease in coronary flow in diabetic mice. The possible role of PGE2 and dysfunctional vasodilation mediated by prostacyclin receptor.Journal of physiology and biochemistry · 2015Article
- Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes.British journal of pharmacology · 2015Review
- Regulation of dipeptidyl peptidase 4 production in adipocytes by glucose.Diabetes, metabolic syndrome and obesity : targets and therapy · 2014Article
- Acute Rho-kinase inhibition improves coronary dysfunction in vivo, in the early diabetic microcirculation.Cardiovascular diabetology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiovascular complications of diabetes result from endothelial dysfunction secondary to persistent hyperglycemia. We investigated potential compensatory mechanisms in the vasculature that oppose endothelial dysfunction in diabetes. BALB/c mice were treated with streptozotocin (STZ) to induce type 1 diabetes (T1D). In mesenteric vascular beds (MVBs), isolated ex vivo from mice treated with STZ for 1 wk, dose-dependent vasorelaxation to acetylcholine (ACh) or sodium nitroprusside was comparable with that in age-matched control mice (CTRL). By contrast, MVBs from mice treated with STZ for 8 wk had severely impaired vasodilator responses to ACh consistent with endothelial dysfunction. Pretreatment of MVBs from CTRL mice with nitric oxide synthase inhibitor nearly abolished vasodilation to ACh. In MVB from 1-wk STZ-treated mice, vasodilation to ACh was only partially impaired by L-N(omega)-arginine methyl ester. Thus, vasculature of mice with T1D may have compensatory nitric oxide-independent mechanisms to augment vasodilation to ACh and oppose endothelial dysfunction. Indeed, pretreatment of MVBs isolated from 1-wk STZ-treated mice with NS-398 [selective cyclooxygenase (COX)-2 inhibitor] unmasked endothelial dysfunction not evident in CTRL mice pretreated without or with NS-398. Expression of COX-2 in MVBs, aortic endothelial cells, and aortic vascular smooth muscle cells from STZ-treated mice was significantly increased (vs. CTRL). Moreover, concentrations of the COX-2-dependent vasodilator 6-keto-prostaglandin F-1alpha was elevated in conditioned media from aorta of STZ-treated mice. We conclude that endothelial dysfunction in a mouse model of T1D is opposed by compensatory up-regulation of COX-2 expression and activity in the vasculature that may be relevant to developing novel therapeutic strategies for diabetes and its cardiovascular complications.
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