Estrogen Effects on Neurite Outgrowth and Cytoskeletal Gene Expression in ERα-Transfected PC12 Cell Lines

Gollapudi, Lakshmi Asritha; Oblinger, Monica M.

doi:10.1006/exnr.2001.7744

Cited by 29 publications

(22 citation statements)

References 62 publications

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“…The production of these proteins is regulated by estradiol-17β and it is possible that this hormone could be responsible for the changes in the expression patterns of at least some of these genes normally considered to have stable patterns. This is supported by several other studies in which some of the genes that are the objects of this study changed expression in response to estradiol-17β: e.g., TUBA1A in human PC12 cell lines transfected with estrogen receptor alpha (Gollapudi and Oblinger, 2001), CTSZ in Sparus aurata macrophages (Liarte et al, 2011), ACTB in mouse uterus (Schroder et al, 2009) and CTSD in O. mykiss white muscle (Cleveland and Weber, 2011). …”

Section: Pattern Of Expression Levels Of Reference Genesmentioning

confidence: 60%

Reference genes to quantify gene expression during oogenesis in a teleost fish

Deloffre

Andrade

Filipe

et al. 2012

Gene

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Section: Pattern Of Expression Levels Of Reference Genesmentioning

confidence: 60%

Reference genes to quantify gene expression during oogenesis in a teleost fish

Deloffre

Andrade

Filipe

et al. 2012

Gene

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“…Previous studies have reported an estrogenic potentiation of NGF-induced neurite outgrowths in PC12 cells stably expressing ER (Gollapudi & Oblinger 2001). Therefore, the aim of the present experiment was to establish whether the A/B domain is involved in such an ER -dependent potentiation.…”

Section: An Increase By 17 E2 Of the Ngf-induced Neurite Outgrowth Ismentioning

confidence: 88%

Estrogen receptor alpha mediates neuronal differentiation and neuroprotection in PC12 cells: critical role of the A/B domain of the receptor

Mérot¹,

Ferrière²,

Debroas³

et al. 2005

Journal of Molecular Endocrinology

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Numerous studies, both in vivo and in vitro, have reported neuronal differentiating and neuroprotective actions of estrogens. Most of these estrogenic effects are mediated through specific receptors termed estrogen receptors. The aim of this study was to assess the importance of the N-terminal A/B domain of the estrogen receptor-alpha (ER ) in its neuronal aspects. Consequently, estrogen effects on (i) the transcriptional activity of target genes, (ii) neuronal differentiation and (iii) neuroprotection in PC12 cells transfected with either a full length form of ER or an A/B domain truncated form (ER CF), have been studied. We demonstrate that the maximal estrogen-induced transcriptional activity of reporter genes requires a full length ER , especially when cells are differentiated. Precisely, the transcriptional activity of ER in differentiated cells relies, predominantly, on the activation function AF-1, located in the A/B domain. Furthermore, in PC12 cells stably expressing ER , 17 -estradiol markedly enhances the neurite outgrowth triggered by treatment with nerve growth factor and protects cells from oxidative shocks induced by depletion of glutathione. These estrogenic effects are not observed in non-transfected cells and in cells transfected with the truncated ER, devoid of the A/B domain. Altogether, these results underline the importance of the A/B domain of ER in both the differentiating and the neuroprotective effects of estrogens.

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“…73 Estrogen can enhance NGF-stimulated neurite sprouting in an ER ␣-dependent manner. 74 In addition, short-term estrogen replacement increases ␤-preprotachykinin mRNA levels in uninjured dorsal root ganglion neurons. 74 Together these observations emphasize the need of basic research to-ward the role of estrogen receptor regulation on the bladder responses to inflammation.…”

Section: Er␤mentioning

confidence: 99%

Gene Expression Profiling of Mouse Bladder Inflammatory Responses to LPS, Substance P, and Antigen-Stimulation

Saban

Nguyen

Hammond

et al. 2002

The American Journal of Pathology

110

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Inflammatory bladder disorders such as interstitial cystitis (IC) deserve attention since a major problem of the disease is diagnosis. IC affects millions of women and isClinical and animal models of acute and chronic urinary bladder inflammation have provided several lines of evidence suggesting a central role of mast cells, sensory nerves, and neurokinin (NK)-1 receptors. Fundamental work regarding the participation of sensory nerves and mast cells in cystitis provides indirect evidence, such as increased numbers of mast cells in the detrusor and submucosa, and morphological evidence of mast cell activation and degranulation. [1][2][3][4] In addition, the extensive tissue remodeling seen in some clinical forms of bladder inflammation such as interstitial cystitis, 4 along with increased urinary levels of histamine and tryptase 5 suggest a role for mast cells. Because both mast cells 6 -8 and NK-1 receptors are increased in bladder biopsies of interstitial cystitis (IC) patients, 9,10 it is tempting to propose a role for sensory peptides-mast cell communication in the pathogenesis of this disorder.Experimentally, we have used classical morphometric analysis and microarray technology to determine the role of mast cells, NK-1 receptors, and bacterial toxins in animal models of cystitis. Time-course experiments indicated early and late genes involved in bladder inflammatory responses. 11 The availability of mice genetically deficient in neurokinin-1 receptor (NK-1R Ϫ/Ϫ ) allowed us to propose a mandatory role of SP receptors in cystitis. 12 We also determined genes that depend on the presence of tissue mast cells for their expression by comparing inflammatory responses in mast cell-deficient (Kit W /

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Estrogen Effects on Neurite Outgrowth and Cytoskeletal Gene Expression in ERα-Transfected PC12 Cell Lines

Cited by 29 publications

References 62 publications

Reference genes to quantify gene expression during oogenesis in a teleost fish

Reference genes to quantify gene expression during oogenesis in a teleost fish

Estrogen receptor alpha mediates neuronal differentiation and neuroprotection in PC12 cells: critical role of the A/B domain of the receptor

Gene Expression Profiling of Mouse Bladder Inflammatory Responses to LPS, Substance P, and Antigen-Stimulation

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