Endothelial Dysfunction in Chronic Myocardial Infarction Despite Increased Vascular Endothelial Nitric Oxide Synthase and Soluble Guanylate Cyclase Expression

Bauersachs, Johann; Bouloumié, Anne; Fraccarollo, Daniela; Hu, Kai; Busse, Rudi; Ertl, Georg

doi:10.1161/01.cir.100.3.292

Cited by 321 publications

(269 citation statements)

References 33 publications

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“…cytokines and oxidative stress). Oxidative stress itself, and superoxide specifically, degrades available NO with formation of peroxynitrate, a toxic metabolite that nitrosylates proteins on tyrosine residues [12,13]. Pro-inflammatory stimuli induce a transition in the endothelium from quiescent to activated state by promoting the expression of vasoactive and pro-inflammatory genes such as iNOS and cyclooxygenase-2 (COX-2).…”

Section: The Endothelium In Chronic Heart Failurementioning

confidence: 99%

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Colombo

Onat

Sabbah

2008

European J of Heart Fail

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Section: The Endothelium In Chronic Heart Failurementioning

confidence: 99%

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Colombo

Onat

Sabbah

2008

European J of Heart Fail

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“…For example, hypertension is associated with increased inhibition of NO signaling by superoxide, whereas NO release remains unaffected. 17 Bauersachs et al 18 also reported that endothelial dysfunction in ischemic heart failure was induced by an increase in vascular superoxide production despite enhanced vascular endothelial nitric oxide synthase (eNOS) and soluble guanylate cyclase expression. Importantly, eNOS is a cytochrome P450 reductase-like enzyme that produces superoxide under certain pathological conditions.…”

Section: Fukuo Et Al Nifedipine Indirectly Upregulates Endothelial Sodmentioning

confidence: 99%

Nifedipine Indirectly Upregulates Superoxide Dismutase Expression in Endothelial Cells via Vascular Smooth Muscle Cell–Dependent Pathways

et al. 2002

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Background-Calcium antagonists normalize endothelial dysfunction in many cardiovascular diseases. There is no known receptor, however, for calcium antagonists in endothelial cells (ECs). We hypothesized that vascular smooth muscle cells (VSMCs) are involved in the mechanism underlying the normalization of endothelial dysfunction by calcium antagonists. Methods and Results-Coculture studies with ECs and VSMCs were performed to determine whether VSMCs mediate modulation of endothelial superoxide dismutase (SOD) activity and expression induced by the calcium antagonist nifedipine. Nifedipine induced upregulation of SOD activity in rat aortic segments but had no effect on SOD expression or activity in ECs or VSMCs cultured individually. When ECs were cocultured with VSMCs, however, nifedipine upregulated SOD expression and activity in ECs. Nifedipine stimulated vascular endothelial growth factor (VEGF) production from VSMCs, and this stimulation of VEGF production was abolished by HOE-140, an antagonist of the bradykinin B 2 receptor. A neutralizing antibody against VEGF inhibited the upregulation of endothelial SOD by nifedipine. In addition, recombinant VEGF induced an increase in the levels of SOD expression in ECs, and supernatant derived from nifedipine-treated VSMCs enhanced NO production from ECs. This increase in NO production by the supernatant was inhibited by preincubation of ECs with SOD antisense oligodeoxyribonucleotides. Conclusions-The

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“…Decreases in ␤ 1 expression were associated with aging, changes in vasodilatory potency, and salt-sensitivity in rats (6). Increases in ␤ 1 subunit level were associated with altered vasodilator response in aortic rings from rats after myocardial infraction (11). Expression of the ␤ 1 subunit was also shown to be developmentally regulated in fish embryos (12) and rat lung and brain (6,13).…”

mentioning

confidence: 92%

CCAAT-binding factor regulates expression of the β ₁ subunit of soluble guanylyl cyclase gene in the BE2 human neuroblastoma cell line

Sharina¹,

Martin²,

Thomas

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Soluble guanylyl cyclase (sGC) is a cytosolic enzyme producing the intracellular messenger cyclic guanosine monophosphate (cGMP) on activation with nitric oxide (NO). sGC is an obligatory heterodimer composed of ␣ and ␤ subunits. We investigated human ␤1 sGC transcriptional regulation in BE2 human neuroblastoma cells. The 5 upstream region of the ␤1 sGC gene was isolated and analyzed for promoter activity by using luciferase reporter constructs. The transcriptional start site of the ␤1 sGC gene in BE2 cells was identified. The functional significance of consensus transcriptional factor binding sites proximal to the transcriptional start site was investigated by site deletions in the 800-bp promoter fragment. The elimination of CCAAT-binding factor (CBF) and growth factor independence 1 (GFI1) binding cores significantly diminished whereas deletion of the NF1 core elevated the transcription. Electrophoretic mobility-shift assay (EMSA) and Western analysis of proteins bound to biotinated EMSA probes confirmed the interaction of GFI1, CBF, and NF1 factors with the ␤1 sGC promoter. Treatment of BE2 cells with genistein, known to inhibit the CBF binding to DNA, significantly reduced protein levels of ␤1 sGC by inhibiting transcription. In summary, our study represents an analysis of the human ␤1 sGC promoter regulation in human neuroblastoma BE2 cells and identifies CBF as a critically important factor in ␤1 sGC expression.

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Endothelial Dysfunction in Chronic Myocardial Infarction Despite Increased Vascular Endothelial Nitric Oxide Synthase and Soluble Guanylate Cyclase Expression

Cited by 321 publications

References 33 publications

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Nifedipine Indirectly Upregulates Superoxide Dismutase Expression in Endothelial Cells via Vascular Smooth Muscle Cell–Dependent Pathways

CCAAT-binding factor regulates expression of the β ₁ subunit of soluble guanylyl cyclase gene in the BE2 human neuroblastoma cell line

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Endothelial Dysfunction in Chronic Myocardial Infarction Despite Increased Vascular Endothelial Nitric Oxide Synthase and Soluble Guanylate Cyclase Expression

Cited by 321 publications

References 33 publications

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Nifedipine Indirectly Upregulates Superoxide Dismutase Expression in Endothelial Cells via Vascular Smooth Muscle Cell–Dependent Pathways

CCAAT-binding factor regulates expression of the β 1 subunit of soluble guanylyl cyclase gene in the BE2 human neuroblastoma cell line

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CCAAT-binding factor regulates expression of the β ₁ subunit of soluble guanylyl cyclase gene in the BE2 human neuroblastoma cell line