Estradiol and raloxifene protect cultured SN4741 neurons against oxidative stress

Biewenga, Eric; Cabell, Leigh; Audesirk, Teresa

doi:10.1016/j.neulet.2004.09.067

Cited by 39 publications

(19 citation statements)

References 29 publications

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“…That the estrogen receptor may not be essential for all estrogen neuroprotection was also suggested by the work of Rothman and coworkers [109], who showed that an estrogen analog (ZYC-5), that lacks activity at estrogen receptors, was neuroprotective via a free radical scavenging mechanism. Other studies have confirmed estrogen neuroprotection against oxidative stress in various cell and animal models of neurodegenerative disorders, most prominently Parkinson's disease, which will be discussed in the next section [110][111][112][113]. Figure 4 shows a summary diagram for the proposed multi-cell, multi-mechanism protection afforded by estrogen in cerebral ischemia.…”

Section: Astrocytes Microglia and Estrogen Neuroprotectionmentioning

confidence: 85%

“…Furthermore, raloxifene did not affect NMDA or AMPA receptor sensitive binding in the striatum in MPTP-treated mice, suggesting that raloxifene does not regulate the concentration of glutamate receptors in MPTP-treated mice [151]. However, work in a clonal substania nigra cell line, SN4741 showed that raloxifene, like E2 can significantly reduce neuronal cell death induced by oxidative stress, suggesting that an antioxidant capability may be involved in at least part of its neuroprotective effects of raloxifene [110].…”

Section: Parkinson's Diseasementioning

confidence: 97%

“…However, a number of studies have shown that estrogen can protect neurons against β-amyloid toxicity [73,185,[195][196][197][198][199], oxidative stress [110][111][112][113]195,200] and excitotoxicity [67,195,201,202], events suggested to participate in the pathology of AD. Additionally, estrogen has been shown to induce dephosphorylation of the tau protein and prevent its hyperphosphorylation in neurons [203].…”

Section: Gene Mutations Aromatase and Potential Mechanisms Of Estrogenmentioning

confidence: 99%

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Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

et al. 2007

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Estrogen is an important hormone signal that regulates multiple tissues and functions in the body. This review focuses on the neurotrophic and neuroprotective actions of estrogen in the brain, with particular emphasis on estrogen actions in the hippocampus, cerebral cortex and striatum. Sex differences in the risk, onset and severity of neurodegenerative disease such as Alzheimer's disease, Parkinson's disease and stroke are well known, and the potential role of estrogen as a neuroprotective factor is discussed in this context. The review assimilates a complex literature that spans research in humans, non-human primates and rodent animal models and attempts to contrast and compare the findings across species where possible. Current controversies regarding the WHI (Women's Health Initiative) study, its ramifications, concerns and the new studies needed to address these concerns are also addressed. Signaling mechanisms underlying estrogen-induced neuroprotection and synaptic plasticity are reviewed, including the important concepts of genomic versus nongenomic mechanisms, types of estrogen receptor involved and their subcellular targeting, and implicated downstream signaling pathways and mediators. Finally, a multicellular mode of estrogen action in the regulation of neuronal survival and neurotrophism is discussed, as are potential future directions for the field.

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Section: Astrocytes Microglia and Estrogen Neuroprotectionmentioning

confidence: 85%

Section: Parkinson's Diseasementioning

confidence: 97%

Section: Gene Mutations Aromatase and Potential Mechanisms Of Estrogenmentioning

confidence: 99%

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Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

et al. 2007

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“…Their role in influencing synaptic plasticity, brain development and memory is well established. Several studies have highlighted the potential neuroprotective action of estrogens against damage produced by acute and chronic injury to the adult brain [16][17][18]. The cellular and molecular mechanisms implicated in these neuroprotective effects however appear to be complex [19][20][21].…”

Section: Discussionmentioning

confidence: 99%

Potential Effects of Hormone Therapy in Type 2 Idiopathic Macular Telangiectasia

et al. 2017

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Purpose: To investigate the influence of hormone therapy with tamoxifen or estrogens on morphological changes in macular telangiectasia (MacTel) type 2 patients as revealed clinically in multiple imaging modalities. Methods: Patients with a history of tamoxifen or estrogen use were selected from the cohort of the MacTel Study. A race-, age- and best-corrected visual acuity-matched group of MacTel participants not under hormone therapy served as the comparison group. The frequencies of typical features of the MacTel phenotype apparent in color fundus, red-free, fluorescein angiographic and optical coherence tomographic images were graded and analyzed statistically. Results: Thirty-nine MacTel patients were included in the analyses, of whom 13 were receiving tamoxifen, 13 estrogens and 13 patients no hormone treatment. Patients treated with estrogens showed significantly fewer breaks in the ellipsoid zone on optical coherence tomography (7 eyes, 29.1%, vs. tamoxifen: 14 eyes, 53.8%, and vs. controls: 14 eyes, 53.8%, p = 0.04 in both analyses, Fisher exact test). Retinal crystalline deposits were significantly more frequent in patients receiving estrogens (12 eyes, 16.2%, vs. 2 eyes, 2.7%, p = 0.003, Fisher exact test). No significant between-group differences were apparent with regard to other features of the phenotype (extent of retinal low reflective spaces, late hyperfluorescence on fluorescein angiography or retinal thickness). Conclusions: Tamoxifen treatment does not seem to accentuate structural changes in patients with MacTel type 2. Treatment with estrogens may exhibit a neuroprotective effect as suggested by the decreased frequency of ellipsoid zone breaks in corresponding patients, although corroborative studies are warranted to confirm these exploratory data.

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“…The well-documented antioxidant effects of tamoxifen, hydroxytamoxifen, and raloxifene in the nervous tissue (Moreira et al 2004, Biewenga et al 2005, Konyalioglu et al 2007, Armagan et al 2009) may be relevant for its neuroprotective actions on Parkinson's disease (Lee et al 2009a,b), cerebral ischemia (Zhang et al 2007, Wakade et al 2008, and other neurodegenerative conditions.…”

Section: Control Of Oxidative Stressmentioning

confidence: 99%

Selective estrogen receptor modulators as brain therapeutic agents

Arévalo¹,

Santos-Galindo²,

Lagunas³

et al. 2010

Journal of Molecular Endocrinology

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Selective estrogen receptor modulators (SERMs), used for the treatment of breast cancer, osteoporosis, and menopausal symptoms, affect the nervous system. Some SERMs trigger neuroprotective mechanisms and reduce neural damage in different experimental models of neural trauma, brain inflammation, neurodegenerative diseases, cognitive impairment, and affective disorders. New SERMs with specific actions on neurons and glial cells may represent promising therapeutic tools for the brain.

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Estradiol and raloxifene protect cultured SN4741 neurons against oxidative stress

Cited by 39 publications

References 29 publications

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

Potential Effects of Hormone Therapy in Type 2 Idiopathic Macular Telangiectasia

Selective estrogen receptor modulators as brain therapeutic agents

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