Stimulation of Membrane-Bound Guanylate Cyclase Activity by 17-β Estradiol

Chen, Zi‐Jiang; Yu, Linda; Chang, Chung-Ho

doi:10.1006/bbrc.1998.9716

Cited by 31 publications

(35 citation statements)

References 14 publications

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“…Moreover, RSVL-induced inhibition of MAPK phosphorylation was insensitive to the E 2 receptor blockers tamoxifen and ICI-182,780l, thereby arguing against a role for estrogen receptors. However, exclusion of`estrogen-like' e¡ects in our system may be premature in light of recent reports suggesting`direct' receptor-independent responses for estradiol [34]. In support, recent studies in E 2 -responsive pituitary tumor cell lines demonstrated the inability of RSVL to bind E 2 receptors, although it mimicked some of the E 2 responses in this system [35].…”

Section: Discussionsupporting

confidence: 51%

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

1999

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In porcine coronary arteries, short-term treatment with resveratrol (RSVL) substantially inhibited MAPK activity (IC 50 = 37 W WM); and immunoblot analyses revealed consistent reduction in the phosphorylation of ERK-1/-2, JNK-1 and p38, at active sites. Endothelin-1 (ET-1), a primary antecedent in coronary heart diseases, enhanced MAPK activity, phosphorylation and nuclear translocation in a concentration-responsive but RSVL-sensitive manner. RSVL had no effect on basal or forskolin-stimulated cAMP levels, a known downregulator of the MAPK cascade. Likewise, inhibition of MAPK by RSVL was not reversed by the estrogen receptor blockers tamoxifen and ICI-182,780. Conversely, RSVL remarkably attenuated basal and ET-1-evoked protein tyrosine phosphorylation. Because MAPKs promote smooth muscle proliferation and contraction, their current inhibition may contribute to the putative protection by RSVL against coronary heart diseases. These effects apparently do not involve interaction with estrogen receptors.z 1999 Federation of European Biochemical Societies.

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Section: Discussionsupporting

confidence: 51%

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

1999

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“…The independence of the neuroprotective effect of estrogen in excitotoxicity and hypoxia from estrogen receptor-mediated pathways or protein synthesis has been demonstrated by several groups (Sawada et al, 1998;Moosmann and Behl, 1999;Zaulyanov et al, 1999). These findings and the immediate efficacy of higher doses of 17 ␤-estradiol indicate that mechanisms unrelated to transcrip- Effect of short-term (1 hr) and long-term (20 hr) pretreatment with 17 ␤-estradiol on the increase in LDH release (⌬ U/ml medium) tional regulation are involved, such as antioxidant properties of estrogens, direct inhibition of NMDA receptors (Weaver et al, 1997), rapid release of calcium from intracellular stores (Beyer and Raab, 1998), stimulation of guanylate cyclase activity (Chen et al, 1998), blockade of calcium entry via L-type calcium channels (Mermelstein et al, 1996), and stabilization of mitochondrial function . In addition, the involvement of a possible membrane-binding site on neurons for various steroids including estrogens is discussed (for review, see Behl and Holsboer, 1999).…”

Section: Discussionmentioning

confidence: 99%

Differential Mechanisms of Neuroprotection by 17 β-Estradiol in Apoptotic versus Necrotic Neurodegeneration

et al. 2001

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The major goal of this study was to compare mechanisms of the neuroprotective potential of 17 ␤-estradiol in two models for oxidative stress-independent apoptotic neuronal cell death with that in necrotic neuronal cell death in primary neuronal cultures derived from rat hippocampus, septum, or cortex. Neuronal apoptosis was induced either by staurosporine or ethylcholine aziridinium (AF64A), as models for necrotic cell death glutamate exposure or oxygen-glucose deprivation (OGD) were applied. Long-term (20 hr) pretreatment (0.1 M 17 ␤-estradiol) was neuroprotective in apoptotic neuronal cell death induced by AF64A (40 M) only in hippocampal and septal neuronal cultures and not in cortical cultures. The neuroprotective effect was blocked by the estrogen antagonists ICI 182,780 and tamoxifen and the phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002. In glutamate and OGD-induced neuronal damage, long-term pretreatment was not effective. In contrast, short-term (1 hr) pretreatment with 17 ␤-estradiol in the dose range of 0.5-1.0 M significantly reduced the release of lactate dehydrogenase and improved morphology of cortical cultures exposed to glutamate or OGD but was not effective in the AF64A model. Staurosporine-induced apoptosis was not prevented by either long-or short-term pretreatment. The strong expression of the estrogen receptor-␣ and the modulation of Bcl proteins by 17 ␤-estradiol in hippocampal and septal but not in cortical cultures indicates that the prevention of apoptotic, but not of necrotic, neuronal cell death by 17 ␤-estradiol possibly depends on the induction of Bcl proteins and the density of estrogen receptor-␣.Key words: apoptosis; necrosis; estradiol; AF64A; staurosporine; oxygen-glucose deprivation; primary neuronal cultures; hippocampus; cortex; septum; Alzheimer' s diseaseThe neuroprotective potential of estrogens has gained increasing attention during the last years. Epidemiological evidence suggests that estrogen replacement therapy for postmenopausal women is associated with an improvement of some measures of cognitive performance, protection against cognitive deterioration, and decreased incidence of Alzheimer's disease

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“…These rapid events may be classified into four main signaling cascade: phospholipase C (PLC)/protein kinase C (PKCs) [100][101][102][103][104][105][106], Ras/Raf/MAPK [72,[107][108][109][110][111][112][113], phosphatidyl inositol 3 kinase (PI3K)/AKT [15,16,80,81,97,[114][115][116][117][118], and cAMP/ protein kinase A (PKA) [104,[119][120][121][122][123].…”

Section: Estrogen Receptor Non-genomic Activ-itymentioning

confidence: 99%

Estrogen Signaling Multiple Pathways to Impact Gene Transcription

Marino¹,

2006

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Steroid hormones exert profound effects on cell growth, development, differentiation, and homeostasis. Their effects are mediated through specific intracellular steroid receptors that act via multiple mechanisms. Among others, the action mechanism starting upon 17 -estradiol (E2) binds to its receptors (ER) is considered a paradigmatic example of how steroid hormones function. Ligand-activated ER dimerizes and translocates in the nucleus where it recognizes specific hormone response elements located in or near promoter DNA regions of target genes. Behind the classical genomic mechanism shared with other steroid hormones, E2 also modulates gene expression by a second indirect mechanism that involves the interaction of ER with other transcription factors which, in turn, bind their cognate DNA elements. In this case, ER modulates the activities of transcription factors such as the activator protein (AP)-1, nuclear factor-B (NF-B) and stimulating protein-1 (Sp-1), by stabilizing DNA-protein complexes and/or recruiting co-activators. In addition, E2 binding to ER may also exert rapid actions that start with the activation of a variety of signal transduction pathways (e.g. ERK/MAPK, p38/MAPK, PI3K/AKT, PLC/PKC). The debate about the contribution of different ER-mediated signaling pathways to coordinate the expression of specific sets of genes is still open. This review will focus on the recent knowledge about the mechanism by which ERs regulate the expression of target genes and the emerging field of integration of membrane and nuclear receptor signaling, giving examples of the ways by which the genomic and non-genomic actions of ERs on target genes converge.

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Stimulation of Membrane-Bound Guanylate Cyclase Activity by 17-β Estradiol

Cited by 31 publications

References 14 publications

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

Differential Mechanisms of Neuroprotection by 17 β-Estradiol in Apoptotic versus Necrotic Neurodegeneration

Estrogen Signaling Multiple Pathways to Impact Gene Transcription

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