Estrogens increase the endothelial nitric oxide synthase (ecNOS) mRNA level in LNCaP human prostate carcinoma cells

Grande, Mirtha; Carlström, Kjell; Stege, Reinhard; Pousette, Åke; Faxén, Margareta

doi:10.1002/1097-0045(20001101)45:3<232::aid-pros5>3.0.co;2-4

Cited by 20 publications

(4 citation statements)

References 22 publications

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“…Grande et al . observed that oestrone, as well as 17β‐oestradiol, increased the expression of endothelial NOS in LNCaP human prostate carcinoma cells 38 . These findings, coupled with the present results, suggest that oestrone may stimulate NOS activity in erythrocyte membranes and increase NO production, which could improve the membrane fluidity of erythrocytes.…”

Section: Discussionsupporting

confidence: 83%

Effect of oestrone on membrane fluidity of erythrocytes is mediated by a nitric oxide‐dependent pathway: An electron paramagnetic resonance study

Tsuda

Kinoshita-Shimamoto

Kimura

et al. 2002

Clin Exp Pharma Physio

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1. It has been recognized that hormone replacement therapy (HRT) may have a beneficial effect on protection against cardiovascular diseases. Oestrone is the major component of conjugated equiline oestrogens, which are commonly used in HRT. The present study was performed in order to investigate the effects of oestrone on the membrane fluidity of erythrocytes by means of an electron paramagnetic resonance (EPR) and spin-labelling method. 2. In an in vitro study, oestrone significantly decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (ho/h-1) for 16-nitroxide stearate (16-NS) obtained from EPR spectra of erythrocyte membranes. This finding indicated that oestrone may increase the membrane fluidity and improve the membrane microviscosity of erythrocytes. 3. The effect of oestrone was significantly potentiated by the nitric oxide (NO) donor s-nitroso-N-acetylpenicillamine and the cGMP analogue 8-bromo-cGMP. 4. In contrast, the change in membrane fluidity induced by oestrone was antagonized by the NO synthase inhibitors NG-nitro-l-arginine methyl ester and asymmetric dimethyl-l-arginine. 5. The results of the present study show that oestrone significantly increases membrane fluidity and improves the rigidity of cell membranes, which is partially mediated by a NO- and cGMP-dependent pathway. Furthermore, the data may be consistent with the hypothesis that oestrone could have a beneficial effect on the rheological behaviour of erythrocytes and have a crucial role in the regulation of the microcirculation.

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Section: Discussionsupporting

confidence: 83%

Effect of oestrone on membrane fluidity of erythrocytes is mediated by a nitric oxide‐dependent pathway: An electron paramagnetic resonance study

Tsuda

Kinoshita-Shimamoto

Kimura

et al. 2002

Clin Exp Pharma Physio

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“…Note that nonvascular cells such as osteoblast-like cells (15) and carcinoma cells (152) were also shown to increase eNOS expression in response to E 2 stimulation. These effects are blocked by specific estrogen antagonists like tamoxifen, confirming the role of ER in the changes in eNOS transcript expression.…”

Section: Genomic Regulation Of Enos Expression By Estrogensmentioning

confidence: 93%

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

397

328

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Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in cardiovascular biology explains its growing implication in mechanosensitive aspects of integrated physiology, such as the control of blood pressure variability or the modulation of cardiac remodeling in situations of hemodynamic overload.

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“…Furthermore, it is involved in the regulation of cardiac function and angiogenesis (Grande et al 2000). There are three known isoforms, two are constitutive (NOS1, NOS3) and the third is inducible (NOS2).…”

Section: Introductionmentioning

confidence: 99%

Endothelial nitric oxide synthase gene polymorphisms and prostate cancer risk in Serbian population

Branković

Brajušković

Nikolic

et al. 2013

Int J Experimental Path

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Genome-wide association studies (GWAS) have identified over 46 SNPs associated with human prostate cancer (PCa). Some studies have shown correlation of the nitric oxide synthase (NOS) NOS3 gene polymorphisms with the risk and/or progression of PCa. This study aimed to evaluate the association of NOS3 gene polymorphisms (-786T>C, -764A>G, -714G>T, -690C>T, -649G>A and 894G>T) with PCa risk and progression. 150 patients with PCa, 150 patients with BPH and 100 age-matched healthy controls were recruited in this study. Genotyping of promoter polymorphisms was performed by bi-directional DNA sequencing, and for 894G>T by RFLP analysis. There was no significant association between the alleles and genotypes of these genetic variants and PCa risk. For -786T>C polymorphism, we found that C allele is associated with absence of metastases, assuming dominant genetic model (P = 0.049; OR, 0.50; 95% CI, 0.25-1.00). It was found that, compared with NOS3 -690C>T variant CC genotype, CT and TT genotypes confer decreased risk of developing metastases (dominant model, P = 0.015, OR, 0.24; 95% CI, 0.07-0.88) and show association with low clinical tumour stage, compared with stages T3 and T4 (dominant model, P = 0.046, OR, 0.20; 95% CI, 0.04-1.02). Genetic variants -764A>G, -714G>T, -649G>A were not detected in our study group. There is evidence of an inverse correlation of the NOS3 894G>T minor allele with high serum PSA (>20 ng/ml) (dominant model, P = 0.013, OR, 0.37; 95% CI, 0.17-0.82). Our results suggest that NOS3 gene polymorphisms are genetic susceptibility factors for the progression of PCa and patient outcome.

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Estrogens increase the endothelial nitric oxide synthase (ecNOS) mRNA level in LNCaP human prostate carcinoma cells

Cited by 20 publications

References 22 publications

Effect of oestrone on membrane fluidity of erythrocytes is mediated by a nitric oxide‐dependent pathway: An electron paramagnetic resonance study

Effect of oestrone on membrane fluidity of erythrocytes is mediated by a nitric oxide‐dependent pathway: An electron paramagnetic resonance study

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Endothelial nitric oxide synthase gene polymorphisms and prostate cancer risk in Serbian population

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