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AB002. Guidance of vascular patterning in ocular development and disease

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Annals of Eye Science 2018年第1期 408-408页

作者： Anne Eichmann Departments of Cardiology and Cellular and Molecular Physiology Yale University School of MedicineNew HavenCTUSA Inserm Paris Cardiovascular Research Center ParisFrance

Ocular vessel networks develop in a highly stereotyped fashion.Abnormal ocular angiogenesis is associated with major diseases including age-related macular degeneration and diabetic retinopathy.Better understanding of mechanisms driving angiogenesis is expected to uncover novel targets to prevent vision loss.Capillary growth is driven by endothelial tip cells,which are selected by dynamic interplay between VEGF,Notch and BMP signaling,with VEGF acting as a positive regulator,and Notch and the BMP receptor Alk1 acting as negative regulators of tip cell formation.The concerted interplay between these molecules ensures that appropriate tip cell numbers leading new vessel branches are formed.In addition,guidance receptors including Neuropilins and Roundabout receptors contribute to vascular patterning by regulating VEGF and BMP signaling.Possibilities to target these pathways during pathological ocular neovascularization will be discussed.

关键词： Vascular development VEGF notch and BMP signaling

Trivalent Chromium Modulates Hexosamine Biosynthesis Pathway Transcriptional Activation of Cholesterol Synthesis and Insulin Resistance

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Open Journal of Endocrine and Metabolic Diseases 2013年第4期3卷 1-8页

作者： Brent A. Penque Lixuan Tackett Jeffrey S. Elmendorf departments of cellular and Integrative physiology and Biochemistry and molecular Biology Centers for Diabetes Research and Membrane Biosciences Indiana University School of Medicine Indianapolis USA

Trivalent chromium has long been recognized to benefit carbohydrate and lipid metabolism. Given emerging evidence that suggests chromium improves insulin sensitivity through the maintenance of an optimal level of plasma membrane (PM) cholesterol, we delineated the role of this micronutrient in attenuating hyperinsulinemia-induced cholesterol biosynthesis and insulin resistance. Exposing 3T3-L1 adipocytes to physiological hyperinsulinemia (500 pM 12 h), resulted in a marked impairment in insulin-stimulated glucose transport. Concurrent treatment with chromium in the picolinate form (CrPic, 10 nM 16 h) prevented against glucose transport dysfunction. Insulin signaling was neither impaired by hyperinsulinemia nor amplified by chromium to promote this protective action. Instead, it was found that hyperinsulinemia promoted an increase in PM cholesterol content that was observed to impair the acute ability of insulin to stimulate GLUT4 redistribution to the PM. Chromium prevented against the accumulation of PM cholesterol. Mechanistically, hyperinsulinemia promoted increases in O-GlcNAc modification of specificity protein 1 (Sp1), known to engage a cholesterolgenic response. Subsequent chromatin immunoprecipitation and luciferase assays revealed that hyperinsulinemia increased the binding affinity of Sp1 to the promoter region of Hmgcr, encoding 3-hydroxy 3-methyl-glutaryl-CoA reductase (HMGR), as well as HMGR promoter activity. This resulted in gains in mRNA and protein content of HMGR, with resulting elevations in PM cholesterol content. Moreover, treatment with chromium prevented this transcriptional response. Together, these data suggest a mechanism whereby CrPic affords glycemic health through inhibition of a transcriptional cholesterolgenic program detrimental to insulin action.

关键词： 3T3-L1 Adipocytes GLUT4 HMG-CoA Reductase Hyperinsulinemia Sp1

Dysregulated microRNAs in type 2 diabetes and breast cancer:Potential associated molecular mechanisms

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World Journal of Diabetes 2024年第6期15卷 1187-1198页

作者： Alex Cleber Improta-Caria Filipe Ferrari João Lucas Penteado Gomes Paloma Brasilio Villalta Úrsula Paula RenóSoci Ricardo Stein Edilamar M Oliveira Laboratory of Biochemistry and molecular Biology of the Exercise Physical Education and Sport SchoolUniversity of São PauloSão Paulo 05508-030Brazil Graduate Program in cardiology and Cardiovascular Sciences Federal University of Rio Grande do SulHospital de Clínicas de Porto AlegrePorto Alegre 90035003Brazil Laboratory of Metabolic Disorders(Labdime) School of Applied SciencesUniversity of Campinas-UNICAMPCampinas 13484-350Brazil departments of Internal Medicine Molecular Pharmacology and PhysiologyCenter for Regenerative MedicineUSF Health Heart InstituteMorsani College of MedicineUniversity of South FloridaTampaFL 33602United States

Type 2 diabetes(T2D)is a multifaceted and heterogeneous syndrome associated with complications such as hypertension,coronary artery disease,and notably,breast cancer(BC).The connection between T2D and BC is established through processes that involve insulin resistance,inflammation and other factors.Despite this comprehension the specific cellular and molecular mechanisms linking T2D to BC,especially through microRNAs(miRNAs),remain elusive.miRNAs are regulators of gene expression at the post-transcriptional level and have the function of regulating target genes by modulating various signaling pathways and biological processes.However,the signaling pathways and biological processes regulated by miRNAs that are associated with T2D and BC have not yet been elucidated.This review aims to identify dysregulated miRNAs in both T2D and BC,exploring potential signaling pathways and biological processes that collectively contribute to the development of BC.

关键词： Type 2 diabetes Breast cancer MicroRNAs molecular mechanisms

Histamine 3 receptor activation mediates inhibition of acid secretion during Helicobacter-induced gastritis

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World Journal of Gastrointestinal Pathophysiology 2010年第5期1卷 154-165页

作者： Yana Zavros Nisreen Mesiwala Meghna Waghray Andrea Todisco Arthur Shulkes Juanita L Merchant departments of Internal Medicine-Gastroenterology University of Michigan Department of molecular and cellular physiology University of Cincinnati Department of Surgery Austin and Repatriation Medical CenterUniversity of Melbourne departments of Internal Medicine and molecular and Integrative physiology University of Michigan

AIM:To test the hypothesis that histamine 3 receptor (H3R)activation during Helicobacter infection inhibits gastric acid secretion in vivo and in vitro.METHODS:Helicobacter felis(H.felis)infected and uninfected C57Bl/6 mice were infused with either PBS or the H3 receptor antagonist thioperamide(THIO)for 12 wk.After treatment,mice were analyzed for morphological changes and gastric acid content.Total RNA was prepared from the stomachs of each group and analyzed for changes in somatostatin and gastrin mRNA abundance by real time-polymerase chain reaction(RTPCR).Location of H3 receptors in the stomach was analyzed by co-localization using antibodies specific for the H3 receptor and parietal cell marker H + ,K + -ATPase βsubunit. RESULTS:Inflammation and parietal cell atrophy was observed after 12 wk of H.felis infection.Interestingly, treatment with the H3R antagonist thioperamide(THIO) prior to and during infection prevented H.felis-induced inflammation and atrophy.Compared to the uninfected controls,infected mice also had significantly decreased gastric acid.After eradication of H.felis with THIO treatment,gastric acidity was restored.Compared to the control mice,somatostatin mRNA abundance was decreased while gastrin gene expression was elevated during infection.Despite elevated gastric acid levels, after eradication of H.felis with THIO,somatostatin mRNA was elevated whereas gastrin mRNA was suppressed.Immunofluorescence revealed the presence of H3 receptors on the parietal cells,somatostatin-secreting D-cells as well as the inflammatory cells. CONCLUSION:This study shows that during H.felis infection,gastric acidity is suppressed as a consequence of an inhibitory effect on the parietal cell by H3R activation.The stimulation of gastric mucosal H3Rs increases gastrin expression and release by inhibiting release of somatostatin.

关键词： Gastrin Somatostatin Histamine Parietal

Brucine N-oxide reduces ethanol intake and preference in alcohol-preferring Fawn-Hooded rats

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中国药理学与毒理学杂志 2017年第5期31卷 479-480页

作者： LIANG Jian-hui WEI Shou-peng LI Yu-ling GONG Qi WANG Yan-ting LIANG Hui LIU Qing ZHANG Han-ting CHEN Feng Andrew J LOWRENCE Department of molecular and cellular Pharmacology School of Pharmaceutical Sciences Department of Pharmacology School of Basic Medicine SciencesPeking University Institute of Psycopharmacology Central Institute of Mental HealthUniversity of Heidelberg departments of Behavioral Medicine & Psychiatry and physiology& Pharmacology West Virginia University Health Sciences Center The Florey Institute of Neuroscience and Mental Health University of Melbourne

OBJECTIVE The alcoholism-related social problems have burdened the public health heavily.A better therapy for alcohol dependence as a chronic brain disease is highly required and interests the scientists worldwide. Our group has focused on screening the right drug with low toxicity and a sound curative effect from traditional Chinese medicine. METHODS Alcohol-preferring Fawn-Hooded(FH/Wjd) rat was used as an animal model of alcoholism to evaluate the effects of brucine N-oxide(BNO),an alkoloid naturally existing in the seeds of Strychnos nux-vomica L,on the alcohol-drinking behaviors.Furthermore,its adverse action and toxicity were investigated. RESULTS Treatment with BNO at the doses of 30,50 and 70 mg · kg^(-1)reduced the voluntary alcohol consumption and preference dosedependently and selectively without altering their water intake,total fluid intake,food consumption,body weight as well as sucrose preference. Remarkably,70 mg·kg^(-1)of BNO did suppress the deprivationinduced elevation of alcohol ingestion. Moreover,BNO used at the same doses as above had no influence on locomotion in an open field test and could not result in the place preference effect. CONCLUSION Taken together,BNO is of some significant pharmacological profiles to inhibit symptoms of alcohol dependence with high safety,and thence may be a potential pharmacotherapy.

关键词： brucine N-oxide ethanol

Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy

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Neuroscience Bulletin 2012年第6期28卷 729-736页

作者： Bijan Akbarpour Mohammad Sayyah Vahab Babapour Reza Mahdian Siamak Beheshti Ahmad Reza Kamyab departments of physiology and Pharmacology Pasteur Institute of Iran.Tehran 131694-3551Islamic Republic of Iran Department of physiology Faculty of Veterinary MedicineIslamic Azad UniversityScience and Research BranchTehran 14778-93855Islamic Republic of Iran departments of physiology and Pharmacology Pasteur Institute of IranTehran 131694-3551Islamic Republic of Iran Department of physiology Faculty of Veterinary MedicineTehran UniversityTehran 141996-31111Islamic-Republic of Iran Department of molecular Medicine Biotechnology Research CenterPasteur Institute of Iran Department of Biology Faculty of Science University of IsfahanIsfahan 81746-73441Islamic Republic of Iran

Objective Understanding the molecular and cellular mechanisms underlying epileptogenesis yields new in- sights into potential therapies that may ultimately prevent epilepsy. Gap junctions （GJs） create direct intercellular conduits between adjacent cells and are formed by hexameric protein subunits called connexins （Cxs）. Changes in the expression of Cxs affect GJ communication and thereby could modulate the dissemination of electrical discharges. The hippocampus is one of the main regions involved in epileptogenesis and has a wide network of GJs between different cell types where Cx30 is expressed in astrocytes and Cx32 exists in neurons and oligodendrocytes. In the present study, we evaluated the changes of Cx30 and Cx32 expression in rat hippocampus during kindling epileptogenesis. Methods Rats were stereotaxically implanted with stimulating and recording electrodes in the basolateral amygdala, which was electrically stimulated once daily at afterdischarge threshold. Expression of Cx30 and Cx32, at both the mRNA and protein levels, was measured in the hippocampus at the beginning, in the middle （after acquisition of focal seizures）, and at the end （after establishment of generalized seizures） of the kindling process, by real-time PCR and Western blot. Results Cx30 mRNA expression was upregulated at the beginning of kindling and after acquisition of focal seizures. Then it was downregulated when the animals acquired generalized seizures. Overexpression of Cx30 mRNA at the start of kindling was consistent with the respective initial protein increase. Thereafter, no change was found in protein abundance during kindling. Regarding Cx32, mRNA expression decreased after acquisition of generalized seizures and no other significant change was detected in mRNA and protein abundance during kindling. Conclusion We speculate that Cx32 GJ communication in the hip- pocampus does not contribute to kindling epileptogenesis. The Cx30 astrocytic network localized to perivascular regions in the hippocampus is, however, overexpres

关键词： connexin 30 connexin 32 hippocampus kindling

Site-specific Proteasome Phosphorylation Controls Cell Proliferation and Tumorigenesis

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Site-specific Proteasome Phosphorylation Controls Cell Proli...

Generating Giant Membrane Vesicles from Live Cells with Preserved cellular Properties

中国生物化学与分子生物学会2016年全国学术会议

作者： Xing Guo Xiaorong Wang Zhiping Wang Sourav Banerjee Jing Yang Lan Huang Jack E.Dixon Department of Pharmacology University of California-San Diego Life Sciences Institute Zhejiang University departments of physiology and Biophysics and of Developmental and Cell Biology University of California Division of Biological Sciences University of California-San Diego Department of Neurobiology Zhejiang University School of Medicine departments of cellular and molecular Medicine and of Chemistry and Biochemistry University of California-San Diego

Despite the fundamental importance of proteasomal degradation in cells,little is known about whether and how the 26S proteasome itself is regulated in coordination with various physiological processes.Here we show that the proteasome is dynamically phosphorylated during cell cycle at Thr25 of the 19S subunit Rpt3.CRISPR/Cas9-mediated genome editing,

关键词： Proteasome Phosphorylation DYRK2 Cell Cycle Tumorigenesis CRISPR/Cas9

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Research 2019年第1期2019卷 859-867页

作者： Qiaoling Liu Cheng Bi Jiangling Li Xuejiao Liu Ruizi Peng Cheng Jin Yang Sun Yifan Lyu Hui Liu Huijing Wang Can Luo Weihong Tan molecular Science and Biomedicine Laboratory(MBL) State Key Laboratory of Chemo/Bio-Sensing and ChemometricsCollege of BiologyCollege of Chemistry and Chemical EngineeringAptamer Engineering Center of Hunan ProvinceHunan UniversityChangshaChina Institute of molecular Medicine(IMM) Renji HospitalShanghai Jiao Tong University School of Medicine and School of Chemistry and Chemical EngineeringShanghai Jiao Tong UniversityShanghaiChina departments of Chemistry Physiology and Functional GenomicsMolecular Genetics and Microbiology and Pathology and Laboratory MedicineUF Health Cancer CenterCenter for Research at the Bio/Nano InterfaceUniversity of FloridaGainesvilleFLUSA

Biomimetic giant membrane vesicles,with size and lipid compositions comparable to cells,have been recognized as an attractive experimental alternative to living systems.Due to the similarity of their membrane structure to that of body cells,cell-derived giant plasma membrane vesicles have been used as a membrane model for studying lipid/protein behavior of plasma membranes.However,further application of biomimetic giant membrane vesicles has been hampered by the side-efects of chemical vesiculants and the utilization of osmotic bufer.We herein develop a facile strategy to derive giant membrane vesicles(GMVs)from mammalian cells in biofriendly medium with high yields.Tese GMVs preserve membrane properties and adaptability for surface modifcation and encapsulation of exogenous molecules,which would facilitate their potential biological applications.Moreover,by loading GMVs with therapeutic drugs,GMVs could be employed for drug transport to tumor cells,which represents another step forward in the biomedical application of giant membrane vesicles.Tis study highlights biocompatible GMVs with biomimicking membrane surface properties and adaptability as an ideal platform for drug delivery strategies with potential clinical applications.

关键词： attractive similarity preserve

Adrenomedullin and endocrine control of immune cells during pregnancy

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cellular & molecular Immunology 2014年第5期11卷 456-459页

作者： Brooke C Matson Kathleen M Caron departments of Cell Biology & physiology University of North Carolina at Chapel Hill Chapel Hill NC USA Genetics University of North Carolina at Chapel Hill Chapel Hill NC USA

The immunology of pregnancy is complex and incompletely understood. Aberrant immune activity in the decidua and in the placenta is believed to play a role in diseases of pregnancy, such as infertility, miscarriage, fetal growth restriction and preeclampsia. Here, we briefly review the endocrine control of uterine natural killer cell populations and their functions by the peptide hormone adrenomedullin. Studies in genetic animal models have revealed the critical importance of adrenomedullin dosage at the maternal-fetal interface, with cells from both the maternal and fetal compartments contributing to essential aspects underlying appropriate uterine receptivity, implantation and vascular remodeling of spiral arteries. These basic insights into the crosstalk between the endocrine and immune systems within the maternal- fetal interface may ultimately translate to a better understanding of the functions and consequences of dysregulated adrenomedullin levels in clinically complicated pregnancies.

关键词： adrenomedullin preeclampsia pregnancy spiral artery remodeling uNK cells