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Book: The identities of membrane steroid receptors

Watson, Cheryl S.

... and other proteins mediating nongenomic steroid action

2003

Author's details	ed. by Cheryl S. Watson
Keywords	Receptors, Steroid ; Receptors, Estrogen
Language	English
Size	XIV, 208 S. : Ill., graph. Darst.
Publisher	Kluwer
Publishing place	Boston u.a
Publishing country	United States
Document type	Book
Note	Includes bibliographical references and index
HBZ-ID	HT013734029
ISBN	1-4020-7344-5 ; 978-1-4020-7344-1
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Environmental estrogen exposures alter molecular signaling in immune cells that promote the development of childhood asthma.

Murakami, Yoko / Fahmy, Sahar / Goldblum, Randall M / Watson, Cheryl S / Midoro-Horiuti, Terumi

Molecular immunology

2023 Volume 157, Page(s) 142–145

Abstract: ... bisphenol A, bisphenol S, or bisphenol A + estradiol. H3K27me3, phosphorylations of EZH2 (pEZH2), AKT (pAKT ...

Abstract	Environmental estrogens (EEs) are associated with an increased prevalence of asthma. These epigenetic alterations of the immune cells may explain the multigenerational effects on asthma development. We hypothesized that exposure to immune cells enhances allergic sensitization by initiating signaling in these cells. Human T cell lines (TIB-152, CCL-119) were exposed to varying concentrations of estradiol, bisphenol A, bisphenol S, or bisphenol A + estradiol. H3K27me3, phosphorylations of EZH2 (pEZH2), AKT (pAKT), and phosphatidylinositide 3-kinase (pPI3K) were assessed. pAKT and pPI3K were decreased in response to some of the concentrations of these exposures in both cell lines. It is likely that EEs exposure to immune cells is one of the factors in the increase in the prevalence of asthma.
MeSH term(s)	Humans ; Asthma ; Estrogens ; Phenols/toxicity ; Estradiol
Chemical Substances	bisphenol A (MLT3645I99) ; Estrogens ; Phenols ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2023-04-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2023.03.023
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Article ; Online: Addiction to a bad idea, especially in low- and middle-income countries: Contributory health insurance.

Yazbeck, Abdo S / Soucat, Agnes L / Tandon, Ajay / Cashin, Cheryl / Kutzin, Joseph / Watson, Julia / Thomson, Sarah / Nguyen, Son Nam / Evetovits, Tamas

Social science & medicine (1982)

2023 Volume 320, Page(s) 115168

Abstract: Despite limited evidence of successful development and implementation of contributory health insurance and low and middle income countries, many countries are in the process implementing such schemes. This commentary summarizes all available evidence on ... ...

Abstract	Despite limited evidence of successful development and implementation of contributory health insurance and low and middle income countries, many countries are in the process implementing such schemes. This commentary summarizes all available evidence on the limitations of contributory health insurance including the lack of good theoretical underpinning and the considerable evidence of inequity and fragmentation created by such schemes. Moreover, the initiation of a contributory health insurance scheme has not been found to increase revenues to the health sector or help health countries achieve universal health coverage. Low and middle income countries can improve equity and efficiency of the health sector by replacing out-of-pocket spending with pre-paid pooling mechanisms, but that is best done through budget transfers and not by contributory insurance that links payment to sub-population entitlements.
MeSH term(s)	Humans ; Developing Countries ; Insurance, Health ; Health Expenditures ; Universal Health Insurance
Language	English
Publishing date	2023-02-21
Publishing country	England
Document type	Journal Article
ZDB-ID	4766-1
ISSN	1873-5347 ; 0037-7856 ; 0277-9536
ISSN (online)	1873-5347
ISSN	0037-7856 ; 0277-9536
DOI	10.1016/j.socscimed.2022.115168
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Article ; Online: Nongenomic effects of estradiol vs. the birth control estrogen ethinyl estradiol on signaling and cell proliferation in pituitary tumor cells, and differences in the ability of R-equol to neutralize or enhance these effects.

Saraf, Manish Kumar / Jeng, Yow-Jiun / Watson, Cheryl S

Steroids

2019 Volume 168, Page(s) 108411

Abstract: Ethinyl estradiol ( ... ...

Abstract	Ethinyl estradiol (EE
MeSH term(s)	Equol ; Estradiol ; Ethinyl Estradiol
Chemical Substances	Ethinyl Estradiol (423D2T571U) ; Estradiol (4TI98Z838E) ; Equol (531-95-3)
Language	English
Publishing date	2019-05-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80312-1
ISSN	1878-5867 ; 0039-128X
ISSN (online)	1878-5867
ISSN	0039-128X
DOI	10.1016/j.steroids.2019.01.008
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Article ; Online: Xenoestrogen interference with nongenomic signaling actions of physiological estrogens in endocrine cancer cells.

Watson, Cheryl S / Koong, Luke / Jeng, Yow-Jiun / Vinas, Rene

Steroids

2018 Volume 142, Page(s) 84–93

Abstract: Rapid nongenomic signaling by estrogens (Es), initiated near the cell membrane, provides new explanations for the potent actions of environmental chemicals that imperfectly mimic physiological Es. These pathways can affect tumor growth, stabilization, or ...

Abstract	Rapid nongenomic signaling by estrogens (Es), initiated near the cell membrane, provides new explanations for the potent actions of environmental chemicals that imperfectly mimic physiological Es. These pathways can affect tumor growth, stabilization, or shrinkage via a number of signaling streams such as activation/inactivation of mitogen-activated protein kinases and caspases, generation of second messengers, and phospho-triggering of cyclin instability. Though prostate cancers are better known for their responsiveness to androgen deprivation, ∼17% of late stage tumors regress in response to high dose natural or pharmaceutical Es; however, the mechanisms at the cellular level are not understood. More accurate recent measurements show that estradiol (E
MeSH term(s)	Cell Line, Tumor ; Cell Survival ; Endocrine Gland Neoplasms/metabolism ; Endocrine Gland Neoplasms/pathology ; Estrogens/metabolism ; Humans ; Male ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Signal Transduction
Chemical Substances	Estrogens
Language	English
Publishing date	2018-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80312-1
ISSN	1878-5867 ; 0039-128X
ISSN (online)	1878-5867
ISSN	0039-128X
DOI	10.1016/j.steroids.2018.06.014
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Article ; Online: Direct estradiol and diethylstilbestrol actions on early- versus late-stage prostate cancer cells.

Koong, Luke Y / Watson, Cheryl S

The Prostate

2014 Volume 74, Issue 16, Page(s) 1589–1603

Abstract: Background: Diethylstilbestrol (DES) and other pharmaceutical estrogens have been used at ≥ µM concentrations to treat advanced prostate tumors, with successes primarily attributed to indirect hypothalamic-pituitary-testicular axis control mechanisms. ... ...

Abstract	Background: Diethylstilbestrol (DES) and other pharmaceutical estrogens have been used at ≥ µM concentrations to treat advanced prostate tumors, with successes primarily attributed to indirect hypothalamic-pituitary-testicular axis control mechanisms. However, estrogens also directly affect tumor cells, though the mechanisms involved are not well understood. Methods: LAPC-4 (androgen-dependent) and PC-3 (androgen-independent) cell viability was measured after estradiol (E2) or DES treatment across wide concentration ranges. We then examined multiple rapid signaling mechanisms at 0.1 nM E2 and 1 µM DES optima including levels of: activation (phosphorylation) for mitogen-activated protein kinases, cell-cycle proteins, and caspase 3, necroptosis, and reactive oxygen species (ROS). Results: LAPC-4 cells were more responsive than PC-3 cells. Robust and sustained extracellular-regulated kinase activation with E2 , but not DES, correlated with ROS generation and cell death. c-Jun N-terminal kinase was only activated in E2-treated PC-3 cells and was not correlated with caspase 3-mediated apoptosis; necroptosis was not involved. The cell-cycle inhibitor protein p16(INK4A) was phosphorylated in both cell lines by both E2 and DES, but to differing extents. In both cell types, both estrogens activated p38 kinase, which subsequently phosphorylated cyclin D1, tagging it for degradation, except in DES-treated PC-3 cells. Conclusions: Cyclin D1 status correlated most closely with disrupted cell cycling as a cause of reduced cell numbers, though other mechanisms also contributed. As low as 0.1 nM E2 effectively elicited these mechanisms, and its use could dramatically improve outcomes for both early- and late-stage prostate cancer patients, while avoiding the side effects of high-dose DES treatment.
MeSH term(s)	Apoptosis/drug effects ; Caspase 3/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Survival/drug effects ; Cyclin D1/metabolism ; Diethylstilbestrol/pharmacology ; Dose-Response Relationship, Drug ; Estradiol/pharmacology ; Estrogens/pharmacology ; Humans ; Male ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Neoplasm Staging ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Reactive Oxygen Species/metabolism
Chemical Substances	Cell Cycle Proteins ; Estrogens ; Reactive Oxygen Species ; Cyclin D1 (136601-57-5) ; Estradiol (4TI98Z838E) ; Diethylstilbestrol (731DCA35BT) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2014-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604707-5
ISSN	1097-0045 ; 0270-4137
ISSN (online)	1097-0045
ISSN	0270-4137
DOI	10.1002/pros.22875
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Article ; Online: Mothers' Experiences Interacting with Infants after Traumatic Childbirth.

Beck, Cheryl Tatano / Watson, Sue

MCN. The American journal of maternal child nursing

2019 Volume 44, Issue 6, Page(s) 338–344

Abstract: Purpose: The purpose of this study is to describe experiences of mothers interacting with their infants after traumatic childbirth.: Study design and methods: A descriptive phenomenological method guided by Dahlberg, Dahlberg, and Nystrom's ... ...

Abstract	Purpose: The purpose of this study is to describe experiences of mothers interacting with their infants after traumatic childbirth. Study design and methods: A descriptive phenomenological method guided by Dahlberg, Dahlberg, and Nystrom's reflective lifeworld research was used. Women were recruited through Trauma and Birth Stress (TABS), a charitable trust in New Zealand, whose mission is to provide support for women who have experienced traumatic childbirth. Data were collected via an electronic survey. Women were asked to describe how their traumatic births affected their caring for and interactions with their infants and any other children they may have. Results: Eighteen women representing six countries across the globe participated. Four constituents of mothers' experiences interacting with their infants after traumatic births were identified: feelings of numbness and detachment, crying and anger, distressing cognitive changes, and limited outside social interactions. Clinical implications: To help women struggling with the aftermath of their traumatic birth, nurses first need to identify them. Clinicians need to be attentive to symptoms such as a withdrawn, dazed look, and appearing distanced from their infants. Prior to hospital discharge after childbirth, women should be given opportunities to share their perceptions of their birth to determine if they view it as traumatic. Interventions should be started as soon as possible in this fragile mother-infant dyad to prevent long-term consequences.
MeSH term(s)	Adult ; Female ; Humans ; Infant, Newborn ; Middle Aged ; Mother-Child Relations/psychology ; Mothers/psychology ; New Zealand ; Parturition/psychology ; Pregnancy ; Qualitative Research ; Stress, Psychological/complications ; Stress, Psychological/etiology ; Stress, Psychological/psychology
Language	English
Publishing date	2019-09-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	605601-5
ISSN	1539-0683 ; 0361-929X
ISSN (online)	1539-0683
ISSN	0361-929X
DOI	10.1097/NMC.0000000000000565
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Article ; Online: Bisphenol S disrupts estradiol-induced nongenomic signaling in a rat pituitary cell line: effects on cell functions.

Viñas, René / Watson, Cheryl S

Environmental health perspectives

2013 Volume 121, Issue 3, Page(s) 352–358

Abstract: ... thereby initiating nongenomic signaling. Bisphenol S (BPS) is an alternative to BPA in plastic ...

Abstract	Background: Bisphenol A (BPA) is a well-known endocrine disruptor that imperfectly mimics the effects of physiologic estrogens via membrane-bound estrogen receptors (mERα, mERβ, and GPER/GPR30), thereby initiating nongenomic signaling. Bisphenol S (BPS) is an alternative to BPA in plastic consumer products and thermal paper. Objective: To characterize the nongenomic activities of BPS, we examined signaling pathways it evoked in GH3/B6/F10 rat pituitary cells alone and together with the physiologic estrogen estradiol (E2). Extracellular signal-regulated kinase (ERK)- and c-Jun-N-terminal kinase (JNK)-specific phosphorylations were examined for their correlation to three functional responses: proliferation, caspase activation, and prolactin (PRL) release. Methods: We detected ERK and JNK phosphorylations by fixed-cell immunoassays, identified the predominant mER initiating the signaling with selective inhibitors, estimated cell numbers by crystal violet assays, measured caspase activity by cleavage of fluorescent caspase substrates, and measured PRL release by radioimmunoassay. Results: BPS phosphoactivated ERK within 2.5 min in a nonmonotonic dose-dependent manner (10-15 to 10-7 M). When combined with 10-9 M E2, the physiologic estrogen's ERK response was attenuated. BPS could not activate JNK, but it greatly enhanced E2-induced JNK activity. BPS induced cell proliferation at low concentrations (femtomolar to nanomolar), similar to E2. Combinations of both estrogens reduced cell numbers below those of the vehicle control and also activated caspases. Earlier activation of caspase 8 versus caspase 9 demonstrated that BPS initiates apoptosis via the extrinsic pathway, consistent with activation via a membrane receptor. BPS also inhibited rapid (≤ 1 min) E2-induced PRL release. Conclusion: BPS, once considered a safe substitute for BPA, disrupts membrane-initiated E2-induced cell signaling, leading to altered cell proliferation, cell death, and PRL release.
MeSH term(s)	Animals ; Cell Line ; Enzyme Activation ; Estradiol/physiology ; Phenols/toxicity ; Phosphorylation ; Pituitary Gland/cytology ; Pituitary Gland/drug effects ; Pituitary Gland/metabolism ; Prolactin/metabolism ; Protein Kinases/metabolism ; Radioimmunoassay ; Rats ; Signal Transduction/drug effects ; Sulfones/toxicity
Chemical Substances	Phenols ; Sulfones ; Estradiol (4TI98Z838E) ; bis(4-hydroxyphenyl)sulfone (80-09-1) ; Prolactin (9002-62-4) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2013-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/ehp.1205826
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Article ; Online: Usability and acceptability of oral-based HCV self-testing among key populations: a mixed-methods evaluation in Tbilisi, Georgia.

Fajardo, Emmanuel / Watson, Victoria / Kumwenda, Moses / Usharidze, Dali / Gogochashvili, Sophiko / Kakhaberi, David / Giguashvili, Ana / Johnson, Cheryl C / Jamil, Muhammad S / Dacombe, Russell / Stvilia, Ketevan / Easterbrook, Philippa / Ivanova Reipold, Elena

BMC infectious diseases

2022 Volume 22, Issue 1, Page(s) 510

Abstract: Background: Hepatitis C virus self-testing (HCVST) is an additional approach that may expand access to HCV testing. We conducted a mixed-methods cross-sectional observational study to assess the usability and acceptability of HCVST among people who ... ...

Abstract	Background: Hepatitis C virus self-testing (HCVST) is an additional approach that may expand access to HCV testing. We conducted a mixed-methods cross-sectional observational study to assess the usability and acceptability of HCVST among people who inject drugs (PWID), men who have sex with men (MSM) and transgender (TG) people in Tbilisi, Georgia. Methods: The study was conducted from December 2019 to June 2020 among PWID at one harm reduction site and among MSM/TG at one community-based organization. We used a convergent parallel mixed-methods design. Usability was assessed by observing errors made and difficulties faced by participants. Acceptability was assessed using an interviewer-administered semi-structured questionnaire. A subset of participants participated in cognitive and in-depth interviews. Results: A total of 90 PWID, 84 MSM and 6 TG were observed performing HCVST. PWID were older (median age 35 vs 24) and had a lower level of education compared to MSM/TG (27% vs 59%). The proportion of participants who completed all steps successfully without assistance was 60% among PWID and 80% among MSM/TG. The most common error was in sample collection and this was observed more often among PWID than MSM/TG (21% vs 6%; p = 0.002). More PWID requested assistance during HCVST compared to MSM/TG (22% vs 8%; p = 0.011). Acceptability was high in both groups (98% vs 96%; p = 0.407). Inter-reader agreement was 97% among PWID and 99% among MSM/TG. Qualitative data from cognitive (n = 20) and in-depth interviews (n = 20) was consistent with the quantitative data confirming a high usability and acceptability. Conclusions: HCVST was highly acceptable among key populations in Georgia of relatively high educational level, and most participants performed HCVST correctly. A significant difference in usability was observed among PWID compared to MSM/TG, indicating that PWID may benefit from improved messaging and education as well as options to receive direct assistance when self-testing for HCV.
MeSH term(s)	Adult ; Cross-Sectional Studies ; Georgia (Republic)/epidemiology ; HIV Infections/diagnosis ; HIV Infections/epidemiology ; Hepacivirus ; Hepatitis C/diagnosis ; Hepatitis C/epidemiology ; Hepatitis C/psychology ; Homosexuality, Male ; Humans ; Male ; Self-Testing ; Sexual and Gender Minorities ; Substance Abuse, Intravenous/psychology
Language	English
Publishing date	2022-05-31
Publishing country	England
Document type	Journal Article ; Observational Study
ZDB-ID	2041550-3
ISSN	1471-2334 ; 1471-2334
ISSN (online)	1471-2334
ISSN	1471-2334
DOI	10.1186/s12879-022-07484-2
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Article ; Online: Mixtures of xenoestrogens disrupt estradiol-induced non-genomic signaling and downstream functions in pituitary cells.

Viñas, René / Watson, Cheryl S

Environmental health : a global access science source

2013 Volume 12, Page(s) 26

Abstract: ... many intracellular signaling pathways; bisphenol-S is now used as a bisphenol-A substitute. All three compounds ... contaminate the environment globally. We previously showed that bisphenol-S, bisphenol-A, and nonylphenol ... by estradiol, elevated by bisphenol S, and unaffected by mixtures. Intrinsic caspase 9 activity was inhibited ...

Abstract	Background: Our study examines the effects of xenoestrogen mixtures on estradiol-induced non-genomic signaling and associated functional responses. Bisphenol-A, used to manufacture plastic consumer products, and nonylphenol, a surfactant, are estrogenic by a variety of assays, including altering many intracellular signaling pathways; bisphenol-S is now used as a bisphenol-A substitute. All three compounds contaminate the environment globally. We previously showed that bisphenol-S, bisphenol-A, and nonylphenol alone rapidly activated several kinases at very low concentrations in the GH3/B6/F10 rat pituitary cell line. Methods: For each assay we compared the response of individual xenoestrogens at environmentally relevant concentrations (10-15 -10-7 M), to their mixture effects on 10-9 M estradiol-induced responses. We used a medium-throughput plate immunoassay to quantify phosphorylations of extracellular signal-regulated kinases (ERKs) and c-Jun-N-terminal kinases (JNKs). Cell numbers were assessed by crystal violet assay to compare the proliferative effects. Apoptosis was assessed by measuring caspase 8 and 9 activities via the release of the fluorescent product 7-amino-4-trifluoromethylcoumarin. Prolactin release was measured by radio-immunoassay after a 1 min exposure to all individual and combinations of estrogens. Results: Individual xenoestrogens elicited phospho-activation of ERK in a non-monotonic dose- (fM-nM) and mostly oscillating time-dependent (2.5-60 min) manner. When multiple xenoestrogens were combined with nM estradiol, the physiologic estrogen's response was attenuated. Individual bisphenol compounds did not activate JNK, while nonylphenol did; however, the combination of two or three xenoestrogens with estradiol generated an enhanced non-monotonic JNK dose-response. Estradiol and all xenoestrogen compounds induced cell proliferation individually, while the mixtures of these compounds with estradiol suppressed proliferation below that of the vehicle control, suggesting a possible apoptotic response. Extrinsic caspase 8 activity was suppressed by estradiol, elevated by bisphenol S, and unaffected by mixtures. Intrinsic caspase 9 activity was inhibited by estradiol, and by xenoestrogen combinations (at 10-14 and 10-8 M). Mixtures of xenoestrogens impeded the estradiol-induced release of prolactin. Conclusions: In mixtures expected to be found in contaminated environments, xenoestrogens can have dramatic disrupting effects on hormonal mechanisms of cell regulation and their downstream functional responses, altering cellular responses to physiologic estrogens.
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Cell Line ; Cell Proliferation/drug effects ; Environmental Pollutants/toxicity ; Estradiol/metabolism ; Estrogens/metabolism ; Estrogens/toxicity ; Extracellular Signal-Regulated MAP Kinases/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Phenols/toxicity ; Phosphorylation ; Pituitary Gland/drug effects ; Rats ; Signal Transduction ; Sulfones/toxicity
Chemical Substances	Benzhydryl Compounds ; Environmental Pollutants ; Estrogens ; Phenols ; Sulfones ; Estradiol (4TI98Z838E) ; nonylphenol (79F6A2ILP5) ; bis(4-hydroxyphenyl)sulfone (80-09-1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2013-03-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1476-069X
ISSN (online)	1476-069X
DOI	10.1186/1476-069X-12-26
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