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Molecular mechanism of endocrine-disruptive effects induced by Bisphenol A:The role of transmembrane g-protein estrogen receptor 1 and integrin αvβ3

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Journal of Environmental Sciences 2019年第1期31卷 1-13页

作者： Zhiguo Sheng Cong Wang Furong Ren Yuxiang Liu Benzhan Zhu Research Center for Eco-Environmental Sciences Chinese Academy of Sciences University of Chinese Academy of Sciences College of Chemistry and Chemical Engineering Xinjiang Normal University

Bisphenol A(BPA) is one of the highest volume industrial products worldwide and has been widely used to make various products as the intermediates of polycarbonate plastics and epoxy resins.Inevitably, general population has been widely exposed to BPA due to extensive use of BPAcontaining products. BPA has similar chemical structure with the natural estrogen and has been shown to induce a variety of estrogen-like endocrine effects on organism in vivo or in vitro. High doses of BPA tend to act as antagonist of estrogen receptors(ERs) by directly regulating the genomic transcription. However, BPA at environmentally relevant low-dose always disrupt the biological function via a non-genomic manner mediated by membrane receptors, rather than ERs. Although some studies had investigated the non-genomic effects of low-dose BPA, the exact molecular mechanism still remains unclear. Recently, we found that membrane g protein-coupled estrogen receptor 1 and integrin αvβ3 and its relative signal pathways participate in the induction of male germ cell proliferation and thyroid transcription disruption by the low-dose BPA. A profound understanding for the mechanism of action of the environmentally relevant BPA exposure not only contributes to objectively evaluate and predict the potential influence to human health, but also provides theoretical basis and methodological support for assessing health effects trigged by other estrogen-like environmental endocrine disruptors. Based mainly on our recent findings, this review outlines the research progress of molecular mechanism on endocrine disrupting effects of environmental low-dose BPA, existing problems and some consideration for future studies.

关键词： Bisphenol A Low-dose effects g protein-coupled estrogen receptor 1 Integrin ανβ3 Reproductive toxicity Thyroxine interference effect

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Myelin Oligodendrocyte glycoprotein-Igg Contributes to Oligodendrocytopathy in the Presence of Complement, Distinct from Astrocytopathy Induced by AQP4-Igg

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Neuroscience Bulletin 2019年第5期35卷 853-866页

作者： Ling Fang Xinmei Kang Zhen Wang Shisi Wang Jingqi Wang Yifan Zhou Chen Chen Xiaobo Sun Yaping Yan Allan g. Kermode Lisheng Peng Wei Qiu Department of Neurology The Third Affiliated Hospital of Sun Yat-sen University Guangzhou 510000 China Department of Neurology Xuanwu Hospital Capital Medical University Beijing 100053 China Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China College of Life Sciences Shaanxi Normal University Xi’an 710119 China Department of Neurology Centre for Neuromuscular and Neurological Disorders Queen Elizabeth II Medical Centre Sir Charles Gairdner Hospital University of Western Australia Perth WA 6009 Australia

Immunoglobulin g against myelin oligodendrocyte glycoprotein(MOg-Ig g) is detectable in neuromyelitis optica spectrum disorder(NMOSD) without aquaporin-4 Ig g(AQP4-Ig g), but its pathogenicity remains unclear.In this study, we explored the pathogenic mechanisms of MOg-Ig g in vitro and in vivo and compared them with those of AQP4-Ig g. MOg-Ig g-positive serum induced complement activation and cell death in human embryonic kidney(HEK)-293 T cells transfected with human MOg. In C57 BL/6 mice and Sprague-Dawley rats, MOg-Ig g only caused lesions in the presence of complement. Interestingly, AQP4-Ig g induced astroglial damage, while MOgIg g mainly caused myelin loss. MOg-Ig g also induced astrocyte damage in mouse brains in the presence ofcomplement. Importantly, we also observed ultrastructural changes induced by MOg-Ig g and AQP4-Ig g. These findings suggest that MOg-Ig g directly mediates cell death by activating complement in vitro and producing NMOSDlike lesions in vivo. AQP4-Ig g directly targets astrocytes,while MOg-Ig g mainly damages oligodendrocytes.

关键词： Neuromyelitis optica spectrum disorder Aquaporin-4 immunoglobulin g Myelin oligodendrocyte glycoprotein immunoglobulin g Complement-dependent cytotoxicity Transmission electron microscopy

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Control of grain size by g protein signaling in rice

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Journal of Integrative Plant Biology 2019年第5期61卷 533-540页

作者： Ran Xu Na Li Yunhai Li State Key Laboratory of Plant Cell and Chromosome Engineering CAS Center for Excellence in Molecular Plant SciencesInstitute of Genetics and Developmental Biologythe Chinese Academy of SciencesBeijing 100101China The University of Chinese Academy of Sciences Beijing 100039China

Heterotrimeric g proteins are involved in multiple cellular processes in eukaryotes by sensing and transducing various signals. g protein signaling in plants is quite different from that in animals, and the mechanisms of plant g protein signaling are still largely unknown. Several recent studies have provided new insights into the mechanisms of g protein signaling in rice grain size and yield control. In this review,we summarize recent advances on the function of g proteins in rice grain size control and discuss the potential genetic and molecular mechanisms of plant g protein signaling.

关键词： Heterotrimeric g proteins cellular processes in eukaryotes g protein signaling

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gPER agonist g1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2019年第7期14卷 1221-1229页

作者： Zi-Wei Han Yue-Chen Chang Ying Zhou Hang Zhang Long Chen Yang Zhang Jun-Qiang Si Li Li Department of Physiology Medical College of Shihezi University Key Laboratory of Xinjiang Endemic and Ethnic Disease Shihezi University School of Medicine Affiliated Teng Zhou Central People's Hospital Jining Medical University Department of Physiology Jiaxing College of Medicine

Studies have confirmed a strong association between activation of the endoplasmic reticulum stress pathway and cerebral ischemia/reperfusion(I/R) injury.In this study,three key proteins in the endoplasmic reticulum stress pathway(glucose-regulated protein 78,caspase-12,and C/EBP homologous protein) were selected to examine the potential mechanism of endoplasmic reticulum stress in the neuroprotective effect of g protein-coupled estrogen receptor.Female Sprague-Dawley rats received ovariectomy(OVX),and then cerebral I/R rat models(OVX+ I/R) were established by middle cerebral artery occlusion.Immediately after I/R,rat models were injected with 100 μg/kg E2(OVX + I/R +E2),or 100 μg/kg g protein-coupled estrogen receptor agonist g1(OVX + I/R + g1) in the lateral ventricle.Longa scoring was used to detect neurobehavioral changes in each group.Infarct volumes were measured by 2,3,5-triphenyltetrazolium chloride staining.Morphological changes in neurons were observed by Nissl staining.Terminal dexynucleotidyl transferase-mediated nick end-labeling staining revealed that compared with the OVX + I/R group,neurological function was remarkably improved,infarct volume was reduced,number of normal Nissl bodies was dramatically increased,and number of apoptotic neurons in the hippocampus was decreased after E2 and g1 intervention.To detect the expression and distribution of endoplasmic reticulum stress-related proteins in the endoplasmic reticulum,caspase-12 distribution and expression were detected by immunofluorescence,and mRNA and protein levels of glucose-regulated protein 78,caspase-12,and C/EBP homologous protein were determined by polymerase chain reaction and western blot assay.The results showed that compared with the OVX+ I/R group,E2 and g1 treatment obviously decreased mRNA and protein expression levels of glucose-regulated protein 78,C/EBP homologous protein,and caspase-12.However,the g protein-coupled estrogen receptor antagonist g15(OVX + I/R + E2 + g15) could eliminate the effect of E2 on cerebral I/R injury.T

关键词： nerve regeneration cerebral ischemia/reperfusion injury estrogen g protein-coupled estrogen receptor g1 g15 endoplasmic reticulum stress glucose-regulated protein 78 caspase-12 C/EBP homologous protein neuronal apoptosis neural regeneration

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g protein-coupled receptor kinase 2 inhibition improves erectile function through amelioration of endothelial dysfunction and oxidative stress in a rat model of type 2 diabetes

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Asian Journal of Andrology 2019年第1期21卷 74-79页

作者： Zhi-Hua Wan Yuan-Jie Zhang Lin Chen Yong-Lian guo guo-Hao Li Ding Wu Yong Wang Department of Urology The Central Hospital of WuhanTongll Medical CollegeHuazhong University of Science and TechnologyWuhan 430014China

Type 2 diabetes mellitus (T2DM)is a common cause of erectile dysfunction (ED).It has been demonstrated that g protein-coupled receptor kinase 2 (gRK2)overexpression contributes to diabetic endothelial dysfunction and oxidative stress,which also underlies ED in T2DM.We hypothesized that gRK2 overexpressed and attenuated endothelial function of the cavernosal tissue in a rat model of T2DM.T2DM rats were established by feeding with a high-fat diet (HFD)for 2 weeks and then administering two intraperitoneal (IP) injections of a low dose of streptozotocin (STZ),followed by continuous feeding with a HFD for 6 weeks.gRK2 was inhibited by IP injection of paroxetine,a selective gRK2 inhibitor,after STZ injection.Insulin challenge tests,intracavernous pressure (ICP), gRK2 expression,the protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS)pathway,nicotinamide adenine dinucleotide phosphate (NADPH)oxidase subunit gp91phox,nitric oxide (NO),reactive oxygen species (ROS)production,and apoptosis in cavernosal tissue were examined.Less response to insulin injection was observed in T2DM rats 2 weeks after HFD.Markedly increased gRK2 expression,along with impaired Akt/eNOS pathway,reduced NO production,increased gp91phox expression and ROS generation,increased apoptosis and impaired erectile function were found in T2DM rats.inhibition of gRK2 with paroxetine ameliorated Akt/eNOS signaling,restored NO production,downregulated NADPH oxidase,subsequently inhibited ROS generation and apoptosis,and ultimately preserved erectile function.These results indicated that gRK2 upregulation may be an important mechanism underlying T2DM ED,and gRK2 inhibition may be a potential therapeutic strategy for T2DM ED.

关键词： endothelial dysfunction erectile dysfunction g protein-coupled receptor kinase 2 oxidative stress type 2 diabetes mellitus

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Up-regulation of P2X7 Receptors Contributes to Spinal Microglial Activation and the Development of Pain Induced by BmK-I

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Neuroscience Bulletin 2019年第4期35卷 624-636页

作者： Jingjing Zhou Xiaoxue Zhang You Zhou Bin Wu Zhi-Yong Tan Laboratory of Neuropharmacology and Neurotoxicology Shanghai University Shanghai 200444 China Department of Pharmacology and Toxicology and Stark Neurosciences Research Institute Indiana University School of Medicine Indianapolis IN 46202 USA

Previous work has demonstrated that the sensitization of spinal neurons and microglia is important in the development of pain behaviors induced by BmK I,a Na^+ channel activator and a major peptide component of the venom of the scorpion Buthus martensi Karsch(BmK).We found that the expression of P2X7 receptors(P2X7Rs)was up-regulated in the ipsilateral spinal dorsal horn after BmK I injection in rats.P2X7R was selectively localized in microglia but not astrocytes or neurons.Similarly,interleukin 1β(IL-1β)was selectively up-regulated in microglia in the spinal dorsal horn after BmK I injection.Intrathecal injection of P2X7R antagonists largely reduced BmK I-induced spontaneous and evoked pain behaviors,and the up-regulation of P2X7R and IL-1β in the spinal cord.These data suggested that the up-regulation of P2X7Rs mediates microglial activation in the spinal dorsal horn,and therefore contributes to the development of BmK I-induced pain.

关键词： P2X7 receptor BmK I Spinal dorsal horn Interleukin 1β Microglia Brilliant Blue g

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g protein-coupled receptor 37(gPR37) emerges as an important modulator of adenosinergic transmission in the striatum

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Neural Regeneration Research 2019年第11期14卷 1912-1914页

作者： Xavier Morato Rodrigo A. Cunha Francisco Ciruela Unitat de Farmacologia Departament Patologia i Terapeutica ExperimentalFacultat de MedicinaInstituto de Investigacion Biomedica de Bellvitge (IDIBELL)Universitat de BarcelonaL’Hospitalet de LlobregatBarcelonaSpainInstitut de NeurocienciesUniversitat de BarcelonaBarcelonaSpain (Morato X Ciruela F) Center for Neuroscience and Cell Biology (CNC)-Center for Neurosciences and Cell BiologyUniversity of CoimbraCoimbraPortugalFaculty of MedicineUniversity of CoimbraCoimbraPortugal

g protein-coupled receptor 37 (gPR37), also known as parkin associated endothelin-like (Pael) receptor, is an orphan g protein- coupled receptor, which suffers a defective parking ubiquitination in autosomal recessive Parkinson’s disease promoting its endoplasmic reticulum aggregation and stress, neurotoxicity and neuronal death (Takahashi and Imai, 2003). Interestingly, we have demonstrated previously that gPR37 heteromerizes with adenosine A2A receptor (A2AR) in the striatum (Morato et al., 2017;Sokolina et al., 2017).

关键词： g protein-coupled receptor 37(gPR37) important modulator adenosinergic transmission

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Classification of gastric neuroendocrine tumors and its clinicopathologic significance

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World Journal of gastroenterology 1998年第2期4卷 66-69页

作者： Yu, JY Wang, LP Meng, YH Hu, M Wang, JL Bordi, C Navy gen Hosp Dept Pathol Beijing 100037 Peoples R China PLA Beijing Command Area Gen Hosp Beijing Peoples R China Univ Parma I-43100 Parma Italy

ＣｌａｓｓｉｆｉｃａｔｉｏｎｏｆｇａｓｔｒｉｃｎｅｕｒｏｅｎｄｏｃｒｉｎｅｔｕｍｏｒｓａｎｄｉｔｓｃｌｉｎｉｃｏｐａｔｈｏｌｏｇｉｃｓｉｇｎｉｆｉｃａｎｃｅＹＵＪｉＹａｏ１，ＷＡＮＧＬｕＰｉｎｇ２，ＭＥＮＧＹｕ... 详细信息

ＣｌａｓｓｉｆｉｃａｔｉｏｎｏｆｇａｓｔｒｉｃｎｅｕｒｏｅｎｄｏｃｒｉｎｅｔｕｍｏｒｓａｎｄｉｔｓｃｌｉｎｉｃｏｐａｔｈｏｌｏｇｉｃｓｉｇｎｉｆｉｃａｎｃｅＹＵＪｉＹａｏ１，ＷＡＮＧＬｕＰｉｎｇ２，ＭＥＮＧＹｕＨｏｎｇ１，ＨＵＭｅｎｇ１，ＷＡ...

关键词： stomach neoplasms/pathology neuroendocrine tumors/pathology carcinoid tumor/pathology gastritis, atrophic g cell immunohistochemistry microsocopy, electron

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EV71 infection correlates with viral Igg preexisting at pharyngolaryngeal mucosa in children

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Virologica Sinica 2015年第2期30卷 146-152页

作者： Jingchang Xue Yaoming Li Xiaoyi Xu Jie Yu Hu Yan Huimin Yan Changzhou Center for Disease Control and Prevention Mucosal Immunity Research group State Key Laboratory of VirologyWuhan Institute of VirologyChinese Academy of Sciences

Enterovirus 71(EV71) infection causes severe central nervous system damage, particularly for children under the age of 5 years old, which remains a major public health burden worldwide. Clinical data released that children may be repeatedly infected by different members in enterovirus and get even worsen. Mucosa, especially epithelium of alimentary canal, was considered the primary site of EV71 infection. It has been elusive whether the preexsiting viral antibody in mucosa plays a role in EV71 infection. To answer this question, we respectively measured viral antibody response and EV71 RNA copy number of one hundred throat swab specimens from clinically confirmed EV71-infected children. The results released that low-level of mucosal Ig g antibody against EV71 broadly existed in young population. More importantly, it further elucidated that the children with mucosal preexsiting EV71 Ig g were prone to be infected, which suggested a former viral Ig g mediated enhancement of viral infection in vivo.

关键词： EV71 clinical infection mucosal Ig g VP1 VP2 3D

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Differentially expressed long noncoding RNAs and regulatory mechanism of LINC02407 in human gastric adenocarcinoma

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World Journal of gastroenterology 2019年第39期25卷 5973-5990页

作者： Li-Li Zhou Yan Jiao Hong-Mei Chen Li-Hua Kang Qi Yang Jing Li Meng guan ge Zhu Fei-Qi Liu Shuang Wang Xue Bai Yan-Qiu Song Cancer Center The First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina Department of Hepatobiliary and Pancreatic Surgery The First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina Department of Radiology The First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina

BACKgROUND Long noncoding RNAs(lncRNAs)have been identified to play important roles in the development and progression of various tumors,including gastric cancer(gC).However,the molecular role of lncRNAs in gC progression remains unclear.AIM To investigate the differential expression of lncRNAs in human gC and elucidate the function and regulatory mechanism of LINC02407.METHODS The Cancer genome Atlas database was used to investigate the involvement of lncRNAs in gC.Quantitative real-time polymerase chain reaction was used to estimate the relative expression level of LINC02407 in gC tissues and cells.Functional experiments including CCK8 assay,apoptosis assay,wound healing assay,and transwell assay were used to investigate the effect of LINC02407 on gC cells.Some microRNAs were predicted and verified via bioinformatics analysis and the luciferase reporter system.Predictive analysis and Western blot assay were used to analyze the expression of related proteins.RESULTS Many differentially expressed lncRNAs were identified in gC,and some of them including LINC02407 can affect the survival.LINC02407 was upregulated in tumor tissues compared with adjacent tissues.HgC-27 cells showed the highest LINC02407 expression and HaCaT cells exhibited the lowest expression.Different experiment groups were constructed using LINC02407 overexpressing plasmids and related siRNAs.The results of functional experiments showed that LINC02407 can promote the proliferation,migration,and invasion of gC cells but inhibit apoptosis.Luciferase reporter assay showed that hsa-miR-6845-5p and hsa-miR-4455 was downstream regulated by LINC02407.Western blot analysis showed that adhesion g protein-coupled receptor D1(ADgRD1)was regulated by the LINC02407-miR-6845-5p/miR-4455-ADgRD1 pathways.CONCLUSION LINC02407 plays a role in gC through the LINC02407-miR-6845-5p/miR-4455-ADgRD1 pathways,and thus,it may be an important oncogene and has potential value in gC diagnosis and treatment.

关键词： gastric cancer Long noncoding RNAs LINC02407 Adhesion g proteincoupled receptor D1 MicroRNA-6845-5p MicroRNA-4455

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