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17β-estradiol,through activating the G protein-coupled estrogen receptor,exacerbates the complication of benign prostatic hyperplasia in type 2 diabetes mellitus patients by inducing prostate proliferation

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Journal of Pharmaceutical Analysis 2024年第9期14卷 1372-1386页

作者： Tingting Yang Zhen Qiu Jiaming Shen Yutian He Longxiang Yin Li Chen Jiayu Yuan Junjie Liu Tao Wang Zhenzhou Jiang Changjiang Ying Sitong Qian Jinfang Song Xiaoxing Yin Qian Lu Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy Xuzhou Medical UniversityXuzhouJiangsu221004China Department of Urology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu221006China Department of Pharmacy The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu221006China New Drug Screening Center Jiangsu Center for Pharmacodynamics Research and EvaluationChina Pharmaceutical UniversityNanjing210009China Department of Endocrinology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu221006China Department of Pharmacy The Affiliated Hospital of Jiangnan UniversityWuxiJiangsu214000China

Benign prostatic hyperplasia(BPH)is one of the major chronic complications of type 2 diabetes mellitus(T2DM),and sex steroid hormones are common risk factors for the occurrence of T2DM and *** profiles of sex steroid hormones are simultaneously quantified by LC-MS/MS in the clinical serum of patients,including simple BPH patients,newly diagnosed T2DM patients,T2DM complicated with BPH patients and matched healthy *** G protein-coupled estrogen receptor(GPER)inhibitor G15,GPER knockdown lentivirus,the YAP1 inhibitor verteporfin,YAP1 knockdown/overexpression lentivirus,targeted metabolomics analysis,and Co-IP assays are used to investigate the molecular mechanisms of the disrupted sex steroid hormones homeostasis in the pathological process of T2DM complicated with *** homeostasis of sex steroid hormone is disrupted in the serum of patients,accompanying with the proliferated prostatic epithelial cells(PECs).The sex steroid hormone metabolic profiles of T2DM patients complicated with BPH have the greatest degrees of separation from those of healthy *** 17β-estradiol(E2)is the key contributor to the disrupted sex steroid hormone homeostasis,and is significantly positively related to the clinical characteristics of T2DM patients complicated with *** GPER by E2 via Hippo-YAP1 signaling exacerbates high glucose(HG)-induced PECs proliferation through the formation of the YAP1-TEAD4 *** or inhibition of GPER-mediated Hippo-YAP1 signaling suppresses PECs proliferation in HG and E2 co-treated BPH-1 *** anti-proliferative effects of verteporfin,an inhibitor of YAP1,are blocked by YAP1 overexpression in HG and E2 co-treated BPH-1 *** E2/GPER/Hippo/YAP1 signaling may be effective at delaying the progression of T2DM complicated with BPH by inhibiting PECs proliferation.

关键词： Sex steroid hormone homeos tasis Proliferation 17β-estradiol G protein-coupled estrogen receptor T2DM complicated with BPH Hippo-YAP1 signaling

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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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17β-estradiol up-regulates UDP-glucuronosyltransferase 1A9 expression via estrogen receptor α

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Acta Pharmaceutica Sinica B 2016年第5期6卷 504-509页

作者： Sung-joon Cho Miaoran Ning Yanyan Zhang Leah H.Rubin Hyunyoung Jeong Department of Biopharmaceutical Sciences College of PharmacyUniversity of Illinois at Chicago Department of Pharmacy Practice College of PharmacyUniversity of Illinois at Chicago Department of Psychiatry University of Illinois at Chicago

UDP-glucuronosyltransferase 1A9(UGT1A9) is a major phase II enzyme responsible for elimination of drugs and endogenous *** data have shown increased elimination of UGT1A9 substrates in pregnant women or oral contraceptive users,but the role of estrogen in the regulation of UGT1A9 expression remains *** this study,we investigated the effect of 17β-estradiol(E2) on UGT1A9 expression and the role of ERα in the transcriptional regulation of UGT1A9.E2 significantly increased UGT1A9 promoter activity in Hep G2 cells in the presence of ERα.UGT1A9 induction by E2 was abrogated by antiestrogen ICI182,780 in Hep G2 cells that constitutively express ERα.Results from transient transfection of ERα mutants into Hep G2 cells demonstrated that mutation at DNA-binding domain of ERα abrogates increased UGT1A9 promoter activity by *** and mutation assays of UGT1A9 promoter revealed a putative ERE located within -2262/-1987 *** of healthy human liver tissues revealed significantly higher UGT1A9 expression in women as compared to ***,these findings provide a mechanistic basis for the previous clinical reports and may shed a light on identifying sources for inter-individual variability in UGT1A9-mediated drug metabolism.

关键词： UGT1A9 17β-estradiol Estrogen receptor Drug metabolism Sex difference

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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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17β-estradiol inhibits TGF-β-induced collagen gel contraction mediated by human Tenon fibroblasts via Smads and MAPK signaling pathways

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International Journal of Ophthalmology(English edition) 2023年第9期16卷 1441-1449页

作者： Cheng-Cheng Yang Meng-Jie Liu Yun-Ze-Peng Li Zheng-Hua Xu Yang Liu Zi-Han Guo Bin-Hui Li Xiu-Xia Yang Department of Ophthalmology the Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual ScienceSchool of MedicineXiamen UniversityXiamen 361000Fujian ProvinceChina

AIM:To investigate the impact of 17β-estradiol on the collagen gels contraction(CGC)and inflammation induced by transforming growth factor(TGF)-βin human Tenon fibroblasts(HTFs).METHODS:HTFs were three-dimensionally cultivated in type I collagen-generated gels with or without TGF-β(5 ng/mL),17β-estradiol(12.5 to 100μmol/L),or progesterone(12.5 to 100μmol/L).Then,the collagen gel diameter was determined to assess the contraction,and the development of stress fibers was analyzed using immunofluorescence *** and gelatin zymography assays were used to analyze matrix metalloproteinases(MMPs)and tissue inhibitors of metalloproteinases(TIMPs)being released into culture ***-linked immunosorbent assay(ELISA)and reverse transcription-quantitative polymerase chain reaction(RT-PCR)were used to detect interleukin(IL)-6,monocyte chemoattractant proteins(MCP)-1,and vascular endothelial growth factor(VEGF)in HTFs at the translational and transcriptional *** phosphorylation levels of Sma-and Mad-related proteins(Smads),mitogen-activated protein kinases(MAPKs),and protein kinase B(AKT)were measured by *** analysis was performed using either the Tukey-Kramer test or Student’s unpaired t-test to compare the various ***:The CGC caused by TGF-βin HTFs was significantly inhibited by 17β-estradiol(25 to 100μmol/L),and a statistically significant difference was observed when comparing the normal control group with 17β-estradiol concentrations exceeding 25μmol/L(P17β-estradiol became evident 24h after administration and peaked at 72h(P17β-estradiol attenuated the formation of stress fibers,and the production of MMP-3 and MMP-1 in HTFs stimulated by TGF-β.The expression of MCP-1,IL-6,and VEGF mRNA and protein in HTFs were suppressed by 100μmol/L 17β-estradiol(P<0.01).Additionally,the phosphorylation of Smad2 Smad3,p38,and extracellula

关键词： Tenon fibroblasts transforming growth factor-β 17β-estradiol fibrosis wound healing

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Adsorption of 17β-estradiol from aqueous solution by raw and direct/pre/post-KOH treated lotus seedpod biochar

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Journal of Environmental Sciences 2020年第1期32卷 10-23页

作者： Ni Liu Yunguo Liu Guangming Zeng Jilai Gong Xiaofei Tan Jun Wen Shaobo Liu Luhua Jiang Meifang Li Zhihong Yin College of Environmental Science and Engineering Hunan UniversityChangsha 410082P.R.China Key Laboratory of Environmental Biology and Pollution Control Hunan UniversityMinistry of EducationChangsha 410082China College of Agriculture Guangxi UniversityNanning 530005China School of Architecture and Art Central South UniversityChangsha 410082China School of Metallurgy and Environment Central South UniversityChangsha 410083China

Five biochars derived from lotus seedpod(LSP)were applied to examine and compare the adsorption capacity of 17β-estradiol(E2)from aqueous *** effect of KOH activation and the order of activation steps on material properties were *** effect of contact time,initial concentration,p H,ionic strength and humic acid on E2 adsorption were investigated in a batch adsorption *** results demonstrated that the pseudo second-order model fitted the experimental data best and that adsorption equilibrium was reached within 20 *** efficiency of E2 removal increased with increasing E2 concentration and decreased with the increase of ionic strength.E2 adsorption on LSP-derived biochar(BCs)was influenced little by humic acid,and slightly affected by the solution p H when its value ranged from 4.0 to 9.0,but considerably affected at p H *** environmental temperature is favorable for E2 ***,π–πinteractions,monolayer adsorption and electrostatic interaction are the possible adsorption *** studies indicated that KOH activation and the order of activation steps had significant impacts on the ***-treated biochar exhibited better adsorption capacity for E2 than direct treated,pretreated,and raw LSP *** biochar at higher temperature improved E2 *** excellent performance of BCs in removing E2 suggested that BCs have potential in E2 treatment and that the biochar directly treated by KOH would be a good choice for the treatment of E2 in aqueous solution,with its advantages of good efficiency and simple technology.

关键词： 17β-estradiol Lotus seedpod derived biochar Activation order Pre-or post-treatment Adsorption

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Extraction of 17β-estradiol in water using non-imprinted polymer submicron particles in membrane filters

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Journal of Environmental Sciences 2010年第11期22卷 1820-1825页

作者： Yiyan Li Edward P. C. Lai Institute of Environmental Science Carleton University 1125 Colonel By Drive Ottawa Ontario K1S 5B6 Canada. Department of Chemistry Carleton University 1125 Colonel By Drive Ottawa Ontario K1S 5B6 Canada

17β-estradiol （E2） is an endocrine disrupting chemical of harm to both animals and human beings at a low concentration level （ng/L）. It cannot be completely removed by wastewater treatments, and is often detected in both environment and drinking waters. The purpose of this feasibility study, towards environmental engineering in the field of water analysis and treatment, was to remove E2 by extraction using non-imprinted polymer （NIP） submicron particles. Experimental results showed that 0.5 mg/L of E2 could be completely extracted by adding 10 mg of NIP particles directly into 10 mL of water. However, the extraction efficiency decreased to 64% for 100 mL of water. prefilling the NIP particles inside a membrane filter showed a potential for water treatment of a large volume, requiring no effort to distribute the particles uniformly in the water. High extraction efficiency （80 ± 10）% for E2 was achieved for 100 mL of water. A total mass of 0.29 mg E2 was extracted from 1000 mL of water containing 0.8 mg/L E2 （by using only 10 mg of NIP particles）. Both efficiency and mass capacity can be increased, by scaling up the amount of NIP particles, towards environmental engineering applications.

关键词： 17β-estradiol non-imprinted polymer submicron particles membrane filter pollution abatement technology

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A Novel Chemiluminescence Immunoassay Using Solid-Phase Antigen for Free 17β-estradiol in Human Serum

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Chinese Journal of Chemistry 2011年第11期29卷 2520-2524页

作者：祁嫒媛陈惠林珍陈国南林金明 Department of Chemistry Fuzhou University Fuzhou Fujian 350002 China Department of Chemistry Tsinghua University Beijing 100084 China

A high-performance chemiluminescence immunoassay, with long-term durability, good precision and time- saving, was proposed for the detection of free 17β-estradiol （E2） in human serum. Ninety-six microplates were coated with bovine serum albumin conjugated E2 antigen as solid phase for the immunoassay. The E2-BSA antigen coated on the microplate and the E2 antigen in the sample competed for the binding sites on the horseradish peroxi- dase （HRP） labeled anti-E2 antibody. Chemiluminescence reaction was subsequently carried out by HRP catalyzing luminol-H2O2 substrates, and the chemiluminescence intensity was inversely proportional to the amount of analyte in human sera samples. The concentration of immunoreagents, immunoreaction time, and other relevant variable conditions upon the immunoassay were studied and optimized. The proposed method exhibited detection limit as low as 5.94× 10^-3 μg·L^-1 in a linear detection range from 0.01 to 1.00μg·L^-1 good recoveries between 105% and 108%, and high precision with intra- and inter-assay coefficients between 7.9% and 14.3%.

关键词： immunoassay 17β-estradiol antigen indirect competitive immunoreaction horseradish peroxidase

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Upregulation of SIRT1 by 17β-estradiol depends on ubiquitin-proteasome degradation of PPAR-γ mediated by NEDD4-1

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Protein & Cell 2013年第4期4卷 310-321页

作者： Limin Han Pan Wang Ganye Zhao Hui Wang Meng Wang Jun Chen Tanjun Tong Peking University Research Center on Aging Peking University Health Science CenterBeijing 100191China Department of Biochemistry&Molecular Biology School of Basic MedicinePeking University Health Science CenterBeijing 100191China

17β-estradiol (E2) treatment of cells results in an upregulation of SIRT1 and a down-regulation of PPARγ. The decrease in PPARγ expression is mediated by increased degradation of PPARγ. Here we report that PPARγ is ubiquitinated by HECT E3 ubiquitin ligase NEDD4-1 and degraded, along with PPARγ, in response to E2 stimulation. The PPARγ interacts with ubiquitin ligase NEDD4-1 through a conserved PPXY-WW binding motif. The WW3 domain in NEDD4-1 is critical for binding to PPARΓ. NEDD4-1 overexpression leads to PPARγ ubiquitination and reduced expression of PPARγ. Conversely, knockdown of NEDD4-1 by specific siRNAs abolishes PPARΓ ubiquitination. These data indicate that NEDD4-1 is the E3 ubiquitin ligase responsible for PPARγ ubiquitination. Here, we show that NEDD4-1 delays cellular senescence by degrading PPARΓ expression. Taken together, our data show that E2 could upregulate SIRT1 expression via promoting the PPARΓ ubiquitination-proteasome degradation pathway to delay the process of cell senescence.

关键词： 17β-estradiol PPARγ senescence SIRT1 ubiquitination

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iTRAQ-based analysis of 17β-estradiol induced proteome in Chinese tongue sole Cynoglossus semilaevis

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Journal of Oceanology and Limnology 2019年第5期37卷 1659-1668页

作者： ZHU Ying LI Yangzhen LI Hailong WANG Lei ZHANG Ning LIU Yang MENG Liang XU Xiwen DONG Zhongdian WEI Min GUO Hua CUI Zhongkai LI Xihong SHAO Changwei XU Wenteng Key Laboratory of Sustainable Development of Marine Fisheries Ministry of AgricultureYellow Sea Fisheries Research InstituteChinese Academy of Fishery SciencesQingdao 266071China Laboratory for Marine Fisheries Science and Food Production Processes Qingdao National Laboratory for Marine Science and TechnologyQingdao 266237China Research Institute of Metabolic Disease Qingdao UniversityQingdao 266003China

The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sole ( Cynoglossus semilaevis ), 17β-estradiol (E2) can be used reportedly to induce the feminization of fi sh, although the detailed regulatory network remained elusive. We treated the tongue sole fry before sex diff erentiation with E2 (10 and 30 μg/L) to identify potential targets of E2 in Chinese tongue sole. The E2 treatment indeed induced genetic male fi sh sex-reversal to phenotypic female. Using an iTRAQ-based comparative proteomic analysis, 409 proteins that diff erentially expressed after E2 induction were identifi ed, including 259 up-regulated and 150 down-regulated proteins. Furthermore, 19 diff erentially expressed proteins identifi ed in the comparative proteomic analysis were selected to assess their transcription and eight of them exhibited the same tendency. Functions of the eight proteins included mainly nucleotide and protein binding. Interestingly, a far upstream element-binding protein 3-like isoform exhibited the signifi cant upregulation both at transcription and translation levels after E2 treatment. This work identifi ed a set of candidate proteins for E2 response and deepened our understanding of E2 regulatory mechanism.

关键词： Cynoglossus semilaevis 17β-estradiol sex reversal proteome iTRAQ analysis

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