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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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estrogen caused a calcium rise via activation of the g protein-coupled estrogen receptor in SH-SY5Y cells

Estrogen caused a calcium rise via activation of the G prote...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者： Xiaowei Ding Po gao Li Dong Qian Li guohua Zhang Weifang Rong Department of Physiology Shanghai Jiaotong University School of Medicine

The g protein-coupled estrogen receptor 1(gPER1,also known as gPR30),is a gs or gi/o coupled gPCR and has been reported to bind 17β-estradiol(E2)to mediate the non-genomic estrogenic ***1 has been detected in several brain regions,including the hypothalamus,the brainstem and the spinal ***,the signaling mechanisms of this receptor in neuronal cells are yet to be *** present study was aimed to test the hypothesis that activation of gPER1 might induce a change in intracellular calcium level in SH-SY5Y cells,a human neuroblastoma cell *** presence of gPER1 was confirmed by western blot and immunofluorescence ***,the receptor appeared to be enriched on the golgi apparatus,rather than the plasma *** then performed calcium imaging and tested the effects of E2 and g-1,a synthetic gPER1 *** E2and g-1 evoked rapid(within seconds)and robust calcium rises in concentration-dependent manners(0.01μM for E2 and 0.1μM for g-1).The effects were blocked by the gPER1 antagonist g-15(3μM).In the absence of extracellular calcium,both E2 and g-1 only gave rise to minimal calcium ***,Cd Cl2(200μM),a non-selective inhibitor of the voltage-gated calcium channels,failed to block the increase of intracellular calcium induced by E2 or *** contrast,thapsigargin(10μM),which supposedly caused store depletion,prevented the calcium response to E2 and *** IP3R inhibitor,2-APB(100μM),also partially blocked the effects of E2 or *** results demonstrate that activation of gPER1 may induce a rapid calcium rise that appears to be dependent on both calcium entry and calcium *** channels mediating the calcium influx remain to be *** rise of intracellular calcium following activation of gPER1 may underlie some of the rapid effects of estrogen in the central nervous system.

关键词： estrogen g protein-coupled estrogen receptor intracellular calcium SH-SY5Y cells

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The Role of gPER in Sepsis-Induced Myocardial Cell Damage and 28-Day Mortality Risk

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Yangtze Medicine 2024年第3期8卷 57-71页

作者： Jiangfeng Tang Jiangqin Liu Department of Cardiology The First Affiliated Hospital Jiangxi Medical College of Nanchang University Nanchang China Department of Emergency Gaoxin Branch of The First Affiliated Hospital Jiangxi Medical College of Nanchang University Nanchang China

Purpose: The role of gPER in sepsis-induced myocardial cell injury and its potential impact on the risk of death within 28 days in sepsis. Methods: An in vitro experiment was conducted to establish a sepsis-induced myocardial cell model. H9C2 myocardial cells were treated with 10 μg/ml lipopolysaccharide (LPS) for 24 hours. The effects of different concentrations of the gPER agonist g1 (1, 3, and 10 μmol/L) on cell viability, expression of inflammatory markers, cell apoptosis, and the NF-κB pathway were evaluated. A Mendelian randomization analysis was conducted using Single Nucleotide Polymorphism (SNPs) related to the gPER gene as instrumental variables to investigate the causal relationship between the gPER gene variations and sepsis (28-day death). Results: The results indicate that the group treated with LPS showed a significant decrease in myocardial cell viability, an increase in concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), higher apoptosis rates, and increased phosphorylation levels of NF-κB p65 (p-P65/P65) and IκB-α (p-IκB-α/IκB-α) compared to the control group (P κB pathway. However, genetic evidence did not show a causal relationship between gPER gene variations and sepsis (28-day death) (P κB pathway. However, genetic evidence did not show a causal relationship between gPER gene variations and sepsis (28-day death).

关键词： g protein-coupled estrogen receptor Sepsis-Induced Cardiomyopathy Inflammation and Apoptosis Sepsis (28-Day death) Mendelian Randomization

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gPER-expressing neurons in the RVM play a major role in descending regulation of itch

GPER-expressing neurons in the RVM play a major role in desc...

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2019中国生理学会学术年会暨张锡钧基金第十五届全国青年优秀生理学学术论文交流会及第十三届全国青年生理学工作者学术会议

作者：高婷 Jiahong Qian Xiaowei Ding Po gao guohua Zhang Weifang Rong Department of Anatomy and Physiology College of Basic Medical SciencesShanghai Jiao Tong University School of Medicine

Itch is an unpleasant cutaneous sensation that triggers a strong urge to *** significant breakthroughs in understanding the molecular and cellular mechanisms of itch at the spinal and peripheral levels,little is known about the role of the supraspinal descending system in itch ***, we report that a neuronal population which specifically express the g protein-coupled estrogen receptor(gPER) in the rostral ventromedial medulla(RVM), an essential part of the descending pain modulation system, were significantly activated in itch *** found that itch-evoked scratching behavior was impaired after activating gPER+ neurons in the RVM, while ablating or suppressing these neurons increased itch-induced scratching ***, gPER-deficient mice and rats exhibited hypersensitivity to mechanical and chemical itch, a phenotype reversible by μ type opioid receptor(MOR)***, significant MOR phosphory lation in the RVM was detected in chronic itch models in wild-type but not in gPER-/-*** results indicate that RVM gPER+ neurons might exert an "anti-pruritus" function through regulating opioid signaling pathways.

关键词： itch g protein-coupled estrogen receptor μtype opioid receptor rostral ventromedial medulla

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gPER and IgF-1R mediate the anti-inflammatory effect of genistein against lipopolysaccharide-induced nigrostriatal injury

GPER and IGF-1R mediate the anti-inflammatory effect of geni...

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2019中国生理学会学术年会暨张锡钧基金第十五届全国青年优秀生理学学术论文交流会及第十三届全国青年生理学工作者学术会议

作者：张梅 Zhong-Rui Du Wen-Fang Chen Department of Physiology and Pathophysiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological DisordersSchool of Basic MedicineQingdao University

Objective Neuroinflammation plays an important role in the pathogenesis of Parkinson’s disease(PD).The present study was designed to investigate the anti-inflammatory and neuroprotective mechanism of genistein in LPS-induced PD rat *** LPS was injected into the substantia nigra to establish a rat inflammatory model of *** dopamine(DA) content in the striatum was studied by *** numbers of TH-ir neurons and the activation of microglia in the SNpc were detected by *** inflammatory factors protein expressions were detected by western blot and *** genistein pretreatment could ameliorate the apomorphine-induced rotational behavior in LPS-induced inflammatory PD rat *** attenuated LPS-induced decrease of the contents of DA and its metabolites in striatum as well as the loss of TH-IR neurons in the lesioned side of *** gPER antagonist g15 or IgF-1 R antagonist JB-1 blocked the neuroprotective effects of ***, genistein significantly inhibited LPS-induced microglial activation and production of TNF-α, IL-1β, iNOS and *** of gPER or IgF-1 R by g15 or JB1 could attenuate the anti-inflammatory effects of ***, genistein treatment could inhibit the LPS-induced activation of NF-κB and MAPKs signaling pathways in the lesioned side of SN, which could also be blocked by g15 or *** genistein inhibits microglial inflammatory responses and protects nigral dopaminergic neurons via gPER and IgF-1 R signaling pathways.

关键词： genistein g protein-coupled estrogen receptor insulin-like growth factor 1 receptor neuroinflammation Parkinson’s disease

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gPER is involved in the anti-inflammatory effects of genistein in BV2 microglial cells

GPER is involved in the anti-inflammatory effects of geniste...

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中国神经科学学会第十二届全国学术会议

作者： Zhong-Rui DU Liang-Jie YUAN Wen-Fang CHEN Department of Physiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders Medical College of Qingdao University

Objective genistein is an isoflavonoid phytoestrogen extracted from leguminous plants exerting both estrogen agonist and antagonist activities. The present study hypothesized that the anti-inflammatory effects of genistein against lipopolysaccharide（LPS）-induced BV2 microglial activation might be mediated by membrane estrogen receptor（g-protein coupled estrogen receptor, gPER）. Methods The anti-inflammatory effects of genistein were investigated in LPS-induced microglial activation in murine BV2 cells. g1, the specific agonist of gPER, was used as a positive control. The pharmacological blockade and lentivirus-mediated si RNA knockdown of gPER were used to study the underlying mechanism. Results genistein mimicked the effects of g1 treatment by inhibiting the LPS-induced gene expressions of inflammatory cytokines, including TNF-a, IL-1b, COX-2 and iNOS in BV2 microglial cells. Pretreatment with gPER antagonist g15 or si RNA knockdown of gPER could significantly block the anti-inflammatory effects of genistein and g1. Furthermore, pretreatment with g15 could also block the inhibitory effects of genistein on LPS-induced phosphorylation of JNK, p38, ERK and IkB. Conclusion genistein exerts antin-inflammatory effects in BV2 microglial cells possibly by the activating gPER.

关键词： genistein g protein-coupled estrogen receptor insulin-like growth factor 1 receptor microglia

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