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Zearalenone toxicosis on reproduction as estrogen receptor selective modulator and alleviation of zearalenone biodegradative agent in pregnant sows

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Journal of Animal Science and Biotechnology 2022年第4期13卷 1222-1232页

作者： Jianchuan Zhou Lihong Zhao Shimeng Huang Qingxiu Liu Xiang Ao Yuanpei Lei Cheng Ji Qiugang Ma State Key Laboratory of Animal Nutrition College of Animal Science and TechnologyChina Agricultural UniversityBeijing 100193China Sichuan tieqilishi Food Co. LtdMianyang 610000Sichuan provinceChina.

Background:Zearalenone(ZEA)is a resorcylic acid lactone derivative derived from various Fusarium species that are widely found in food and *** molecular structure of ZEA resembles that of the mammalian hormone 17β-oestradiol,thus zearalenone and its metabolites are known to compete with endogenous hormones for estrogen receptors binding sites and to activate transcription of oestrogen-responsive ***,the effect of long-term low-dose ZEA exposure on the reproductive response to Bacillus subtilis ANSB01G culture for first-parity gilts has not yet been *** study was conducted to investigate the toxic effects of ZEA as an estrogen receptor selective modulator and the alleviating effects of Bacillus subtilis ANSB01G cultures as ZEA biodegraders in pregnant sows during their first ***:A total of 80 first-parity gilts(Yorkshire×Landrace)were randomly assigned to four dietary treatments during gestation:CO(positive control);MO(negative control,246μg ZEA/kg diet);COA(CO+*** ANSB01G culture with 2×10^(9)CFU/kg diet);MOA(MO+*** ANSB01G culture with 2×10^(9)CFU/kg diet).There were 20 replications per treatment with one gilt per *** low-dose ZEA naturally contaminated diets disordered most of reproductive hormones secretion and affected estrogen receptor-αand estrogen receptor-βconcentrations in serum and specific organs and led to moderate histopathological changes of gilts,but did not cause significant detrimental effects on reproductive *** addition of Bacillus subtilis ANSB01G culture to the diet can effectively relieve the competence of ZEA to estrogen receptor and the disturbance of reproductive hormones secretion,and then ameliorate toxicosis of ZEA in ***:Collectively,our study investigated the effects of feeding low-dose ZEA on reproduction in pregnant sows during their first *** low-dose ZEA could modulate estrogen receptor-αand-βconcentrations in specific organs,ca

关键词： Bacillus subtilis ANSB01G estrogen receptor Mycotoxin biodegradation Pregnant sows Reproductive performance ZEA

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estrogen receptorα-mediated signaling inhibits type Ⅰ interferon response to promote breast carcinogenesis

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Journal of Molecular Cell Biology 2023年第7期15卷 59-72页

作者： Li-Bo Cao Zi-Lun Ruan Yu-Lin Yang Nian-Chao Zhang Chuan Gao Cheguo Cai Jing Zhang Ming-Ming Hu Hong-Bing Shu Department of Infectious Diseases Medical Research InstituteZhongnan Hospital of Wuhan UniversityCollege of Life SciencesWuhan UniversityWuhan 430072China Frontier Science Center for Immunology and Metabolism Taikang Center for Life and Medical SciencesWuhan UniversityWuhan 430072China Research Unit of Innate Immune and Inflammatory Diseases Chinese Academy of Medical SciencesWuhan 430072China

estrogen receptorα(ERα)is an important driver and therapeutic target in∼70%of breast *** ERαdrives breast carcinogenesis is not fully *** this study,we show that ERαis a negative regulator of type I interferon(IFN)*** of ERαby its natural ligand estradiol inhibits IFN-β-induced transcription of downstream IFN-stimulated genes(ISGs),whereas ERαdeficiency or the stimulation with its antagonist fulvestrant has opposite ***,ERαinduces the expression of the histone 2A variant H2A.Z to restrict the engagement of the IFN-stimulated gene factor 3(ISGF3)complex to the promoters of ISGs and also interacts with STAT2 to disrupt the assembly of the ISGF3 *** two events mutually lead to the inhibition of ISG transcription induced by type I *** a xenograft mouse model,fulvestrant enhances the ability of IFN-βto suppress ERα^(+)breast tumor ***,clinical data analysis reveals that ERα^(+)breast cancer patients with higher levels of ISGs exhibit higher long-term survival *** together,our findings suggest that ERαinhibits type I IFN response via two distinct mechanisms to promote breast carcinogenesis.

关键词： estrogen receptor type I interferon breast cancer

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Therapeutic Value of estrogen receptorαin Hepatocellular Carcinoma Based on Molecular Mechanisms

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Journal of Clinical and Translational Hepatology 2022年第1期10卷 140-146页

作者： Xiangzhe Meng Xue Liu Second Clinical College Jining Medical UniversityJiningShandongChina Department of Pathology College of Basic MedicineJining Medical UniversityJiningShandongChina

The incidence of hepatocellular carcinoma(HCC)is signifi-cantly lower in women than men,implying that estrogen receptors(ERs)may play an important role in this sex ***,considerable progress has been made in expanding our understanding of the mechanisms of ERs in *** one of the most important ERs,ERαfunctions as a tumor suppressor in the progression of HCC through various pathways,such as STAT3 signaling pathways,lipid metabolism-related signaling pathways,and non-coding ***,the function of ERαwas reduced with the changes of some molecules in the liver,which may develop further into HCC and make it difficult to achieve an effective hormone treatment ***,there are signs that individualized hormone therapy according to the activity of ERαwill overcome this *** on these observa-tions,it is particularly imperative to reassess and extend the function of ERα.In this review,we mainly elucidated molecular mechanisms associated with ERαin HCC and investigated the individualized hormone therapy based on these mechanisms,with the aim of providing new insights for HCC treatment.

关键词： Hepatocellular carcinoma estrogen receptor Molecular mechanism Hormone therapy Precision medicine

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estrogen receptor gene polymorphism in a Chinese population with multiple sclerosis

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Neural Regeneration Research 2011年第19期6卷 1488-1492页

作者： Qingli Sun Ruping Xie Yu Fu Xiaogang Li Dongsheng Fan Department of Neurology Peking University Third Hospital Beijing 100191 China

This study sought to elucidate the role of the Pvull and Xbal polymorphisms of the estrogen receptor gene in 74 Chinese patients with multiple sclerosis, and 95 ethnicity-matched controls, using polymerase chain reaction-restriction fragment-length polymorphism analysis. The results revealed that the P allele of Pvull was significantly more prevalent in multiple sclerosis patients compared with controls （P = 0.019）. While distribution frequencies were significantly increased in female multiple sclerosis patients compared with female controls （P = 0.044）, no significant difference was observed between male patients and controls （P〉 0.05）. Frequencies of Ppxx genotypes were significantly higher in multiple sclerosis patients compared with controls （24.3% vs 12.8%, P = 0.025）. Genotypes and alleles of the estrogen receptor were not associated with age, number of attacks or expanded disability status scale scores of patients with multiple sclerosis. These findings indicate that the Pvull but not the Xbal polymorphism in the estrogen receptor gene is associated with susceptibility to multiple sclerosis in the Chinese population. In addition, women with P allele appear to be particularly susceptible to multiple sclerosis.

关键词： estrogen receptor gene polymorphism multiple sclerosis case-control study

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17β-Estradiol Regulates SKP2 Expression in Cultured Immature Boar Sertoli Cells Mainly via estrogen receptor β,cAMP-PKA and ERK1/2

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Journal of Integrative Agriculture 2014年第4期13卷 827-836页

作者： WANG Xian-zhong ZHU Feng-wei WANG Yong WANG Yi ZHANG Jiao-jiao ZHANG Jia-hua Chongqing Key Laboratory of Forage & Herbivore College of Animal Science and TechnologySouthwest University

estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2 （SKP2） plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β （ERβ）, the cyclic adenosine monophosphate （cAMP）-protein kinase A （PKA） and extracellular signal-regulated kinase （ERK1/2） pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Treatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen （PCNA）, while increasing the protein concentration of p27kip1. However, the effect of ERa antagonist on these parameters was lower than that of ICI 182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1, Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.

关键词： 17β-estradiol Sertoli cell SKP2 estrogen receptor cAMP-PKA ERK1/2

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Quantified gene expression levels for phase Ⅰ/Ⅱ metabolizing enzyme and estrogen receptor levels in benign prostate from cohorts designated as high-risk （UK） versus low-risk （India）for adenocarcinoma at this organ site：a preliminary study

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Asian Journal of Andrology 2010年第2期12卷 203-214页

作者： Paras B. Singh Narasimhan Ragavan Katherine M. Ashton Prabir Basu Sayeed M. Nadeem Caroline M. Nicholson R. K. Gopala Krishna Shyam S. Matanhelia Francis L. Martin Centre for Biophotonics Lancaster Environment Centre Lancaster University Bailrigg Lancaster LA1 4YQ UK Lancashire Teaching Hospitals NHS Trust Fulwood Preston PR2 9HT UK Wockhardt Hospitals ＆ Kidney Institute Kolkata 700029 India

Risk of clinically significant prostate adenocarcinoma （CAP） varies worldwide,although there is a uniform prevalence of latent disease. A hormone-responsive tissue,the prostate possesses the metabolizing capacity to biotransform a variety of environmental procarcinogens or endogenous hormones. Whether such metabolizing capacity or estrogen receptor （ER） status underlies these demographic differences in susceptibility to CaP remains unclear. With appropriate ethical permission,verified-benign tissues were obtained following transurethral resection of the prostate from a high-risk region （n = 12 UK-resident Caucasians） and a typically low-risk region （n = 14 India-resident Asians）. Quantitative gene expression analysis was employed for cytochrome P450 （CYP）1B1,N-acetyltransferase （NAT）1,NAT2,catechol-O-methyl transferase （ COMT）,sulfotransferase （ SULT） 1A1,ERα,ERβ and aromatase （CYP To quantify the presence or absence of CYP1B1,ERα or ERβ,and to identify ther in situ localization,immunohistochemistry was carried out. The two cohorts had reasonably well-matched serum levels of prostate-specific antigen or hormones. Expression levels for the candidate genes investigated were ***,clear differences in protein levels for CYP1B1 and ERβ were noted. Staining for CYP1B1 tended to be nuclear-associated in the basal glandular epithelial cells,and in UK-resident Caucasian tissues was present at a higher （P = 0.006） level compared with that from India-resident Asians. In contrast,a higher level of positive ERβ staining was noted in prostates from India-resident Asians. These study findings point to differences in metabolizing capacity and ER status in benign prostate tissues that might modulate susceptibility to the emergence of clinically significant CaP in demographically distinct populations.

关键词： CYP1B1 estrogen receptor immunohistochemistry inter-ethnic prostate real-time reverse transcriptase-polymerase chain reaction

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Reduced prostate branching morphogenes,s in stromal fibroblast, but not in epithelial, estrogen receptor a knockout mice

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Asian Journal of Andrology 2012年第4期14卷 546-555页

作者： Ming Chen Chiuan-Ren Yeh Chih-Rong Shyr Hsiu-Hsia Lin Iun Da Shuyuan Yeh Departments of Urology and Pathology University of Rochester Medical Center Rochester New York 14642 USA Sex Hormone Research Center China Medical University Hospital Taichung 40402 Taiwan China

Early studies suggested that estrogen receptor alpha （ERa） is involved in estrogen-mediated imprinting effects in prostate development. We recently reported a more complete ERa knockout （KO） mouse model via mating β-actin Cre transgenic mice with floxed ERa mice. These ACTB-ERaKO male mice showed defects in prostatic branching morphogenesis, which demonstrates that ERa is necessary to maintain proliferative events in the prostate. However, within which prostate cell type ERa exerts those important functions remains to be elucidated. To address this, we have bred floxed ERa mice with either fibroblast-specific protein （FSP）-Cre or probasin-Cre transgenic mice to generate a mouse model that has deleted ERa gene in either stromal fibroblast （FSP-ERaKO） or epithelial （pes-ERaKO） prostate cells. We found that circulating testosterone and fertility were not altered in *** and pes-ERaKO male mice. Prostates of FSP-ERaKO mice have less branching morphogenesis compared to that of wild-type littermates. Further analyses indicated that loss of stromal ERa leads to increased stromal apoptosis, reduced expression of insulin-likegrowth factor-1 （IGF-1） and FGFIO, and increased expression of BMP4. Collectively, we have established the first in vivo prostate stromal and epithelial selective ERaKO mouse models and the results from these mice indicated that stromal fibroblast ERa plays important roles in prostatic branching morphogenesis via a paracrine fashion. Selective deletion of the ERa gene in mouse prostate epithelial cells by probasin-Cre does not affect the regular prostate development and homeostasis.

关键词： Cre-loxP estrogen receptor knockout prostate stromal-epithelial interaction

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Association of estrogen receptor Gene Polymorphisms and Primary Biliary Cirrhosis in a Chinese Population： A Case- Control Study

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Chinese Medical Journal 2015年第22期128卷 3008-3014页

作者： Liu Yang Hong Zhang Yan-Fang Jiang Qing-Long Jin Peng Zhang Xu Li Pu-Jun Gao Jun-Qi Niu Department of Hepatology First Hospital Jilin University Changchun Jilin 130021 China National Clinical Research Center of Kidney Diseases Jinling Hospital Nanjing university School of Medicinel Nanjing Jiangsu 210002 China Phase I Clinical Trials Unit First Hospital Jilin University Changchun Jilin 130021 China

Background： Primary biliary cirrhosis （PBC） is a chronic and slowly progressive cholestatic liver disease characterized by destruction of the interlobular bile ducts and a striking female predominance, The aim of this study was to identity associations between estrogen receptor （ESR） gene polymorphisms with the risk of developing PBC and abnormal serum liver tests in a Chinese population. Methods： Thirty-six patients with PBC （case group） and 35 healthy individuals （control group） from the First Hospital of Jilin University were studied. Whole genomic DNA was extracted from all the participants. Three single-nucleotide polymorphisms （rs2234693~ rs2228480, and rs3798577） from ESR1 and two （rs1256030 and rs1048315） from ESR2 were analyzed by a pyrosequencing method. Demographic data and liver biochemical data were collected. Results： Subjects with the T allele at ESR2 rs1256030 had 1.5 times higher risk of developing PBC than those with the C allele （odds ratio [OR] = 2.1277, 95% confidence interval [CI] = 1.1872-4.5517）. Haplotypes TGC of ESRI rs2234693, rs2228480, and rs3798577 were risk thctors for having PBC. The C allele at ESRI rs2234693 was associated with abnormal alkaline phosphatase （OR 5.2469, 95% CI = 1.3704-20.0895） and gamma-glutamyl transferase （OR = 3.4286, 95% CI = 1.0083-13.6578） levels in PBC patients. Conclusions： ESR2 rs1256030 T allele may be a significant risk factor for the development of PBC. Screening for patients with gene polymorphisms may help to make early diagnoses in patients with PBC.

关键词： estrogen receptor Gene Polymorphism Primary Biliary Cirrhosis

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17β-Estradiol Regulates Cultured Immature Boar Sertoli Cell Proliferation via the cAMP-ERK1/2 Pathway and the estrogen receptor β

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Agricultural Sciences in China 2010年第8期9卷 1201-1210页

作者： WANG Xian-zhong ZHAO Bo-chuan ZHOU Yu-lan ZHOU Yin-tao MA Kai-ge ZHANG Jia-hua Chongqing Key Laboratory of Forage ＆ Herbivore College of Animal Science and Technology Southwest University Chongqing 400716P.R. China

estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells via the estrogen receptor β （ERβ） and the cAMP-extracellular signal-regulated kinase （ERK1/2） pathway. Low levels （10-10-10-8 mol L-1） of 17β-estradiol increased cell number, but high levels （10-7-10-6 mol L-1） decreased it （P〈0.05）. Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol （10-6 mol L-l）（P〉0.05）. The effects of 17β-estradiol （10-9 mol L-1） peaked at the first 24 h （P〈0.05）. 17β-estradiol activated ERK1/2 from 5 min to 24 h, but the activiy of ERK1/2 began to decrease after 4 h. Both PD98059 and U0126, two ERK inhibitors, blocked cell division （P〈0.05）. 17β-estradiol （10-10-10-6 mol L-1） dose-dependently increased cAMP production （P 〈 0.05）, and both 17β-estradiol （10-9 mol L-1） and forskolin, which increases cAMP levels, induced cell proliferation and activated ERK1/2 （P〈 0.05）. Rp-cAMP, an antagonist of cAMP, blocked this 17β-estradiol activity （P〈 0.05）. Two estrogen receptor antagonists, ICI 182780 and ERβ antagonist （ERβAnt）, reduced Sertoli cell number, cAMP production and ERK1/2 activation （P〈 0.05）, but ERaAnt did not （P〉 0.05）. Therefore, 17β- estradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.

关键词： 17β-estradiol Sertoli cell cell proliferation estrogen receptor ERK1/2

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Role of interleukin-8 in the progression of estrogen receptor-negative breast cancer

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Chinese Medical Journal 2007年第20期120卷 1766-1772页

作者： YAO Chen LIN Ying YE Cai-sheng BI Jiong ZHU Yi-fan WANG Shen-ming Division of Breast Surgery Department of Surgery First Affiliated Hospital Sun Yat-sen University Guangzhou 510080 China

Background estrogen receptor （ER） is a very important biomarker of breast cancer. ER deletion has been consistently associated with tumor progression, recurrence, metastasis and poor prognosis, but the biological mechanism is still unclear. ER negative breast cancer expresses high levels of interleukin-8 （IL-8）. ER expression can downregulate IL-8 promotor activity. As a multifunctional cytokine, IL-8 has many important biological activities in tumor genesis and development. With the goal of investigating the role of IL-8 in ER-negative breast cancer progression, we applied RNA interference technology to specifically knockdown the IL-8 expression in ER-negative breast cancer cell line MDA-MB-231.Methods Interfering pRNA-IL-8 and the control was transfected into ER（-） MDA-MB-231. The proliferation, cell apotosis, and invasive ability were recorded in transfected, untransfected and negative transfected cells. These cells were injected into nude mice to assess tumorigenicity, proliferation, metastasis and microvessel density （MVD）.Results In vitro, decreased expression of IL-8 was associated with reduced cell invasion （P〈0.001）, but had no effect on cell proliferation （P〉0.05）. In vivo, neutrophils infiltration was significantly inhibited in pRNA-IL-8 transfected cells compared with untransfected and negatively transfected cells （P=0.001, P〈0.001）. Less metastasis was found in transfected cells compared with negatively transfected cells （0% vs 80%, P=0.048）. Nevertheless, we observed less MVD in transfected cells compared with control in nude mice （P〈0.001）.Conclusions IL-8 inhibits ER-negative breast cancer cell growth and promotes its metastasis in vivo, which may be correlated with neutrophils infiltration induced by IL-8.

关键词： breast cancer interleukin-8 estrogen receptor RNA interference

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