0000000000249359

AUTHOR

Christoph V. Suschek

showing 3 related works from this author

Ultraviolet A1 radiation induces nitric oxide synthase-2 expression in human skin endothelial cells in the absence of proinflammatory cytokines.

2001

Skin exposure to ultraviolet radiation from sunlight causes erythema and edema formation as well as inflammatory responses. As some of these ultraviolet-induced effects are potentially mediated by nitric oxide synthases, we examined the role of cytokines and ultraviolet A 1 radiation (340–400 nm) on the expression of the nitric oxide synthase-2 in endothelia of normal human skin biopsies during short-term organ culture as well as expression and activity of the nitric oxide synthase-2 in in vitro cell cultures of human dermal endothelial cells. Both, cytokine challenge (interleukin-1β + tumor necrosis factor-α + interferon-γ) but also ultraviolet A 1 exposure (50 J per cm 2 ) in the absence …

ultraviolet A1Ultraviolet Raysmedicine.medical_treatmentNitric Oxide Synthase Type IIHuman skinInflammationDermatologyBiologyBiochemistryProinflammatory cytokineNitric oxideCell Linechemistry.chemical_compoundInterferon-gammanitric oxidemedicineHumansEndotheliumPromoter Regions GeneticMolecular BiologySkinTumor Necrosis Factor-alphaNitric oxide synthase 2Cell BiologyMolecular biologynitric oxide synthase-2endothelial cellsNitric oxide synthasehealing cytokinesCytokinechemistryEnzyme InductionImmunologybiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomhuman skinInflammation MediatorsNitric Oxide SynthaseInterleukin-1The Journal of investigative dermatology
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Amphotericin B severely affects expression and activity of the endothelial constitutive nitric oxide synthase involving altered mRNA stability

2000

The therapeutic use of the antifungal drug amphotericin B (AmB) is limited due to severe side effects like glomerular vasoconstriction and risk of renal failure during AmB administration. As nitric oxide (NO) has substantial functions in renal autoregulation, we have determined the effects of AmB on endothelial constitutive NO synthase (ecNOS) expression and activity in human and rat endothelial cell cultures. AmB used at concentrations of 0.6 to 1.25 μg ml−1 led to increases in ecNOS mRNA and protein expression as well as NO production. This was the result of an increased ecNOS mRNA half-life. In contrast, incubation of cells with higher albeit subtoxic concentrations of AmB (2.5–5.0 μg ml…

Pharmacologymedicine.medical_specialtybiologyEndotheliumAntifungal drugNitric Oxide Synthase Type IIIPharmacologyNitric oxideNitric oxide synthaseEndothelial stem cellchemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyMechanism of actionchemistryInternal medicineGene expressionmedicinebiology.proteinmedicine.symptomBritish Journal of Pharmacology
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Nitric oxide-mediated inhibition of androgen receptor activity: possible implications for prostate cancer progression.

2006

Chronic inflammation increases the risk of cancer and many cancers, including prostate cancer, arise at sites of chronic inflammation. Inducible nitric oxide synthase (iNOS) is an enzyme dominantly expressed during inflammatory reactions. Although synthesis of high amounts of nitric oxide (NO) by iNOS has been demonstrated in pathophysiological processes, such as acute or chronic inflammation, autoimmune diseases or tumorigenesis, the role of iNOS activity in most of these diseases is poorly understood. Analysing prostate cancer biopsies by immunohistochemistry we found iNOS protein expression in tumor cells strongly paralleled by nitrotyrosine suggesting that iNOS is fully active. In vitro…

MaleCancer Researchmedicine.medical_specialtymedicine.drug_classNitric Oxide Synthase Type IIBiologymedicine.disease_causeNitric OxideProstate cancerProstateInternal medicineCell Line TumorGeneticsmedicineAndrogen Receptor AntagonistsHumansAndrogen Receptor AntagonistsMolecular BiologyReverse Transcriptase Polymerase Chain ReactionCancerProstatic NeoplasmsAndrogenmedicine.diseaseImmunohistochemistryAndrogen receptormedicine.anatomical_structureEndocrinologyTumor progressionReceptors AndrogenDisease ProgressionCarcinogenesisOncogene
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