Intermittent High Glucose Concentrations Reduce Neuronal Precursor
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Endothelial Cells and the IGF System
L A Bach Endothelial cells as IGF targets 54:1 R1–R13 Review Endothelial cells and the IGF system Correspondence 1,2 Leon A Bach should be addressed to L A Bach 1Department of Medicine (Alfred), Monash University, Prahran 3181, Australia Email 2Department of Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne 3004, Australia [email protected] Abstract Endothelial cells line blood vessels and modulate vascular tone, thrombosis, inflammatory Key Words responses and new vessel formation. They are implicated in many disease processes including " insulin-like growth factor atherosclerosis and cancer. IGFs play a significant role in the physiology of endothelial cells " binding protein by promoting migration, tube formation and production of the vasodilator nitric oxide. " receptor These actions are mediated by the IGF1 and IGF2/mannose 6-phosphate receptors and are " endothelial cell modulated by a family of high-affinity IGF binding proteins. IGFs also increase the number " angiogenesis and function of endothelial progenitor cells, which may contribute to protection from atherosclerosis. IGFs promote angiogenesis, and dysregulation of the IGF system may contribute to this process in cancer and eye diseases including retinopathy of prematurity and diabetic retinopathy. In some situations, IGF deficiency appears to contribute to endothelial dysfunction, whereas IGF may be deleterious in others. These differences may be due to tissue-specific endothelial cell phenotypes or IGFs having distinct roles in different phases of vascular disease. Further studies are therefore required to delineate the Journal of Molecular therapeutic potential of IGF system modulation in pathogenic processes. Endocrinology (2015) 54, R1–R13 Journal of Molecular Endocrinology Introduction Insulin-like growth factor 1 (IGF1) and IGF2 are essential metabolically active and regulate vascular tone, thrombosis, for normal pre- and postnatal growth and development inflammatory responses and new vessel formation. -
Contents Supplemental Table 1
Supplementary material Open Heart SUPPLEMENTAL MATERIAL TO “EXPLORATION OF PATHOPHYSIOLOGICAL PATHWAYS FOR INCIDENT ATRIAL FIBRILLATION – THE MALMÖ PREVENTIVE PROJECT” John Molvin, Amra Jujic, Olle Melander, Manan Pareek, Lennart Råstam, Ulf Lindblad, Bledar Daka, Margrét Leósdóttir, Peter M. Nilsson, Michael H. Olsen & Martin Magnusson Contents Supplemental table 1. Unadjusted Cox regression analyses examining all 92 proteins relation to incident atrial fibrillation ................................................................................... 2-3 List of abbreviations……………………………………………………………………………………………………………4 Molvin J, et al. Open Heart 2020; 7:e001190. doi: 10.1136/openhrt-2019-001190 Supplementary material Open Heart Supplemental table 1. Unadjusted Cox regression analyses examining all 92 proteins relation to incident atrial fibrillation Protein Hazard ratio (95% confidence interval) p-value PON3 0.80 (0.72-0.89) 7.3x10-5 IGFBP2 4.47 (1.42-14-1) 0.011 PAI 1.44 (0.65-3.18) 0.371 CTSD 2.45 (1.13-5.30) 0.023 FABP4 1.27 (1.13-1.44) 8.6x10-5 CD163 5.25 (1.14-24.1) 0.033 GAL4 1.30 (1.15-1.47) 3.5x10-5 LDL-receptor 0.81 (0.39-1.69) 0.582 IL1RT2 0.75 (0.24-2.34) 0.614 t-PA 2.75 (1.21-6.27) 0.016 SELE 0.99 (0.51-1.90) 0.969 CTSZ 2.97 (1.00-8.78) 0.050 GDF15 1.41 (1.25-1.59) 9.7x10-9 CSTB 3.75 (1.58-8.92) 0.003 MPO 4.48 (1.73-11.7) 0.002 PCSK9 1.18 (0.73-1.93) 0.501 IGFBP1 2.48 (1.42-4.35) 0.001 RARRES2 64.3 (1.87-2220.8) 0.021 ITGB2 1.01 (0.31-3.29) 0.990 CCL15 3.58 (0.96-13.3) 0.057 SCGB3A2 0.97 (0.71-1.32) 0.839 CHI3L1 1.26 (1.12-1.43) -
Insulin-Like Growth Factor Axis in Pregnancies Affected by Fetal Growth Disorders Aamod R
Nawathe et al. Clinical Epigenetics (2016) 8:11 DOI 10.1186/s13148-016-0178-5 RESEARCH Open Access Insulin-like growth factor axis in pregnancies affected by fetal growth disorders Aamod R. Nawathe1,2, Mark Christian3, Sung Hye Kim2, Mark Johnson1,2, Makrina D. Savvidou1,2 and Vasso Terzidou1,2* Abstract Background: Insulin-like growth factors 1 and 2 (IGF1 and IGF2) and their binding proteins (IGFBPs) are expressed in the placenta and known to regulate fetal growth. DNA methylation is an epigenetic mechanism which involves addition of methyl group to a cytosine base in the DNA forming a methylated cytosine-phosphate-guanine (CpG) dinucleotide which is known to silence gene expression. This silences gene expression, potentially altering the expression of IGFs and their binding proteins. This study investigates the relationship between DNA methylation of components of the IGF axis in the placenta and disorders in fetal growth. Placental samples were obtained from cord insertions immediately after delivery from appropriate, small (defined as birthweight <10th percentile for the gestation [SGA]) and macrosomic (defined as birthweight > the 90th percentile for the gestation [LGA]) neonates. Placental DNA methylation, mRNA expression and protein levels of components of the IGF axis were determined by pyrosequencing, rtPCR and Western blotting. Results: In the placenta from small for gestational age (SGA) neonates (n = 16), mRNA and protein levels of IGF1 were lower and of IGFBPs (1, 2, 3, 4 and 7) were higher (p < 0.05) compared to appropriately grown neonates (n =37).In contrast, in the placenta from large for gestational age (LGA) neonates (n = 20), mRNA and protein levels of IGF1 was not different and those of IGFBPs (1, 2, 3 and 4) were lower (p < 0.05) compared to appropriately grown neonates. -
Supplementary Table 1: Genes Affected by Anoikis. A, Ratio of Signal
Supplementary Table 1: Genes affected by anoikis. a, ratio of signal intensity of nonanchored cells anchorage dependent cells (CasKoSrc) over anchored cells; b, induced by Src transformation of Cx43KO cells; c, decreased by Src transformation of Cx43Ko cells; *, induced by normalization of Src transformed cells by neighboring nontransformed cells. Gene Symbol Probe Set Fold Changea Gene Name increased Selenbp1 1450699_at 23.22 selenium binding protein 1 Dscr1l1 1450243_a_at 10.77 Down syndrome critical region gene 1-like 1 Dscr1l1 1421425_a_at 4.29 Down syndrome critical region gene 1-like 1 Ttyh1 1426617_a_at 6.70 tweety homolog 1 (Drosophila) 5730521E12Rik 1419065_at 6.16 RIKEN cDNA 5730521E12 gene c 6330406I15Rik 1452244_at 5.87 RIKEN cDNA 6330406I15 gene AF067063 1425160_at 5.73 clone L2 uniform group of 2-cell-stage gene family mRNA Morc 1419418_a_at 5.55 microrchidia c Gpr56 1421118_a_at 5.43 G protein-coupled receptor 56 Pax6 1452526_a_at 5.06 paired box gene 6 Tgfbi 1415871_at 3.73 transforming growth factor beta induced Adarb1 1434932_at 3.70 adenosine deaminase RNA-specific B1 Ddx3y 1452077_at 3.30 DEAD (Asp-Glu-Ala-Asp) box polypeptide 3 Y-linked b Ampd3 1422573_at 3.20 AMP deaminase 3 Gli2 1459211_at 3.07 GLI-Kruppel family member GLI2 Selenbp2 1417580_s_at 2.96 selenium binding protein 2 Adamts1 1450716_at 2.80 a disintegrin-like and metalloprotease with thrombospondin type 1 motif 1 Dusp15 1426189_at 2.70 dual specificity phosphatase-like 15 Dpep3 1429035_at 2.60 dipeptidase 3 Sepp1 1452141_a_at 2.57 selenoprotein P plasma -
Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................ -
Trim24-Regulated Estrogen Response Is Dependent on Specific Histone Modifications in Breast Cancer Cells
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 12-2012 TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE MODIFICATIONS IN BREAST CANCER CELLS Teresa T. Yiu Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biochemistry Commons, Cancer Biology Commons, Medicine and Health Sciences Commons, and the Molecular Biology Commons Recommended Citation Yiu, Teresa T., "TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE MODIFICATIONS IN BREAST CANCER CELLS" (2012). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 313. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/313 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE -
IGFBP2 Is a Biomarker for Predicting Longitudinal Deterioration in Renal Function in Type 2 Diabetes
R P Narayanan et al. IGFBP2 predicts renal function in 1–8 1:95 Research diabetes Open Access IGFBP2 is a biomarker for predicting longitudinal deterioration in renal function in type 2 diabetes Correspondence 1 2 1 1 1 Ram P Narayanan ,BoFu , Adrian H Heald , Kirk W Siddals , Robert L Oliver , should be addressed to Julie E Hudson1, Antony Payton3, Simon G Anderson4, Anne White5, R P Narayanan 3,6 1,7 B-202, Clinical Sciences William E R Ollier and J Martin Gibson Building, Salford Royal NHS 1Vascular Research Group 2School of Community Based Medicine 3Centre for Integrated Genomic Medical Research Foundation Trust, Stott Lane, Salford 4Cardiovascular Research Group 5Endocrinology and Diabetes, Faculty of Medical, Human and Life Sciences, M6 8HD, UK The University of Manchester, Manchester M13 9PT, UK 6Salford R&D 7Department of Endocrinology and Email Diabetes, Salford Royal Hospital NHS Foundation Trust, Salford M6 8HD, UK ram.narayanan@manchester. ac.uk Abstract Objective: Insulin-like growth factors are implicated in the development of diabetic nephropathy. Key Words IGF-binding protein 2 (IGFBP2) and IGF2 are expressed in the kidney, but their associations with " IGFBP2 diabetic nephropathy are unclear. We therefore tested the hypothesis that circulating levels of " longitudinal trends IGF2 and IGFBP2 predict longitudinal renal function in individuals with type 2 diabetes. " renal function Design and methods: IGFBP2 and IGF2 measurements were performed in 436 individuals (263 " real-world data males) with type 2 diabetes. Linear mixed-effect regression analysis was used to model the Endocrine Connections relationship between plasma IGFBP2 concentration and longitudinal changes in estimated glomerular filtration rate (eGFR) over an 8-year period. -
Figure S1. Reverse Transcription‑Quantitative PCR Analysis of ETV5 Mrna Expression Levels in Parental and ETV5 Stable Transfectants
Figure S1. Reverse transcription‑quantitative PCR analysis of ETV5 mRNA expression levels in parental and ETV5 stable transfectants. (A) Hec1a and Hec1a‑ETV5 EC cell lines; (B) Ishikawa and Ishikawa‑ETV5 EC cell lines. **P<0.005, unpaired Student's t‑test. EC, endometrial cancer; ETV5, ETS variant transcription factor 5. Figure S2. Survival analysis of sample clusters 1‑4. Kaplan Meier graphs for (A) recurrence‑free and (B) overall survival. Survival curves were constructed using the Kaplan‑Meier method, and differences between sample cluster curves were analyzed by log‑rank test. Figure S3. ROC analysis of hub genes. For each gene, ROC curve (left) and mRNA expression levels (right) in control (n=35) and tumor (n=545) samples from The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer cohort are shown. mRNA levels are expressed as Log2(x+1), where ‘x’ is the RSEM normalized expression value. ROC, receiver operating characteristic. Table SI. Clinicopathological characteristics of the GSE17025 dataset. Characteristic n % Atrophic endometrium 12 (postmenopausal) (Control group) Tumor stage I 91 100 Histology Endometrioid adenocarcinoma 79 86.81 Papillary serous 12 13.19 Histological grade Grade 1 30 32.97 Grade 2 36 39.56 Grade 3 25 27.47 Myometrial invasiona Superficial (<50%) 67 74.44 Deep (>50%) 23 25.56 aMyometrial invasion information was available for 90 of 91 tumor samples. Table SII. Clinicopathological characteristics of The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer dataset. Characteristic n % Solid tissue normal 16 Tumor samples Stagea I 226 68.278 II 19 5.740 III 70 21.148 IV 16 4.834 Histology Endometrioid 271 81.381 Mixed 10 3.003 Serous 52 15.616 Histological grade Grade 1 78 23.423 Grade 2 91 27.327 Grade 3 164 49.249 Molecular subtypeb POLE 17 7.328 MSI 65 28.017 CN Low 90 38.793 CN High 60 25.862 CN, copy number; MSI, microsatellite instability; POLE, DNA polymerase ε. -
Insulin-Like Growth Factor Binding Proteins 4 and 7 Released by Senescent Cells Promote Premature Senescence in Mesenchymal Stem Cells
Citation: Cell Death and Disease (2013) 4, e911; doi:10.1038/cddis.2013.445 OPEN & 2013 Macmillan Publishers Limited All rights reserved 2041-4889/13 www.nature.com/cddis Insulin-like growth factor binding proteins 4 and 7 released by senescent cells promote premature senescence in mesenchymal stem cells V Severino1,2,3,10, N Alessio4,10, A Farina5, A Sandomenico2,3, M Cipollaro4, G Peluso6,7, U Galderisi*,4,6,8,9 and A Chambery*,1,3 Cellular senescence is the permanent arrest of cell cycle, physiologically related to aging and aging-associated diseases. Senescence is also recognized as a mechanism for limiting the regenerative potential of stem cells and to protect cells from cancer development. The senescence program is realized through autocrine/paracrine pathways based on the activation of a peculiar senescence-associated secretory phenotype (SASP). We show here that conditioned media (CM) of senescent mesenchymal stem cells (MSCs) contain a set of secreted factors that are able to induce a full senescence response in young cells. To delineate a hallmark of stem cells SASP, we have characterized the factors secreted by senescent MSC identifying insulin-like growth factor binding proteins 4 and 7 (IGFBP4 and IGFBP7) as key components needed for triggering senescence in young MSC. The pro-senescent effects of IGFBP4 and IGFBP7 are reversed by single or simultaneous immunodepletion of either proteins from senescent-CM. The blocking of IGFBP4/7 also reduces apoptosis and promotes cell growth, suggesting that they may have a pleiotropic effect on MSC biology. Furthermore, the simultaneous addition of rIGFBP4/7 increased senescence and induced apoptosis in young MSC. -
Systematic Elucidation of Neuron-Astrocyte Interaction in Models of Amyotrophic Lateral Sclerosis Using Multi-Modal Integrated Bioinformatics Workflow
ARTICLE https://doi.org/10.1038/s41467-020-19177-y OPEN Systematic elucidation of neuron-astrocyte interaction in models of amyotrophic lateral sclerosis using multi-modal integrated bioinformatics workflow Vartika Mishra et al.# 1234567890():,; Cell-to-cell communications are critical determinants of pathophysiological phenotypes, but methodologies for their systematic elucidation are lacking. Herein, we propose an approach for the Systematic Elucidation and Assessment of Regulatory Cell-to-cell Interaction Net- works (SEARCHIN) to identify ligand-mediated interactions between distinct cellular com- partments. To test this approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor neurons (MNs) by an unknown mechanism. Our integrative analysis that combines proteomics and regulatory network analysis infers the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligand-receptor pair. The inferred deleterious role of APP and DR6 is confirmed in vitro in models of ALS. Moreover, the DR6 knockdown in MNs of transgenic mutSOD1 mice attenuates the ALS-like phenotype. Our results support the usefulness of integrative, systems biology approach to gain insights into complex neurobiological disease processes as in ALS and posit that the proposed methodology is not restricted to this biological context and could be used in a variety of other non-cell-autonomous communication -
IGFBP4 Antibody
Product Datasheet IGFBP4 antibody Catalog No: #38333 Orders: [email protected] Description Support: [email protected] Product Name IGFBP4 antibody Host Species Rabbit Clonality Polyclonal Purification Antibodies were purified by affinity purification using immunogen. Applications WB,IHC,IF Species Reactivity Human,Mouse,Rat Specificity The antibody detects endogenous level of total IGFBP4 antibody. Immunogen Type Recombinant Protein Immunogen Description Recombinant protein of human IGFBP4. Target Name IGFBP4 Other Names BP-4; IBP4; IGFBP-4; HT29-IGFBP; Accession No. Swiss-Prot#: P22692NCBI Gene ID: 3487 SDS-PAGE MW 28kd Concentration 1.0mg/ml Formulation Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Storage Store at -20°C Application Details WB 1:500 - 1:2000IHC 1:50 - 1:100IF 1:50 - 1:200 Images Immunofluorescence analysis of L929 cells using IGFBP4 at dilution of 1:100. Blue: DAPI for nuclear staining. Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 1 Immunohistochemistry of paraffin-embedded rat brain using IGFBP4 at dilution of 1:100 (40x lens). Immunohistochemistry of paraffin-embedded human stomach using IGFBP4 at dilution of 1:100 (40x lens). Western blot analysis of extracts of various cell lines, using IGFBP4 at 1:1000 dilution. Immunohistochemistry of paraffin-embedded mouse brain using IGFBP4 at dilution of 1:100 (40x lens). Background This gene is a member of the insulin-like growth factor binding protein (IGFBP) family and encodes a protein with an IGFBP domain and a thyroglobulin type-I domain. -
Igfbp2 Potentiates Egfr-Stat3 Signaling in Glioma
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 5-2015 IGFBP2 POTENTIATES EGFR-STAT3 SIGNALING IN GLIOMA Yingxuan Chua Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biology Commons, Cancer Biology Commons, Cell Biology Commons, Genomics Commons, and the Medicine and Health Sciences Commons Recommended Citation Chua, Yingxuan, "IGFBP2 POTENTIATES EGFR-STAT3 SIGNALING IN GLIOMA" (2015). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 592. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/592 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. IGFBP2 POTENTIATES EGFR-STAT3 SIGNALING IN GLIOMA By Yingxuan Chua, M.S. APPROVED: ___________________________ Wei Zhang, Ph.D., Advisory Professor ___________________________ Gregory N. Fuller, M.D., Ph.D. ___________________________ Oliver Bogler, Ph.D. ___________________________ Paul J. Chiao, Ph.D. ___________________________ Frederick F. Lang Jr, M.D. ___________________________ Zhimin Lu, M.D., Ph.D. APPROVED: ________________________ Dean, The University of Texas Graduate School of Biomedical Sciences at Houston IGFBP2 POTENTIATES EGFR-STAT3 SIGNALING IN GLIOMA A DISSERTATION Presented to the faculty of The University of Texas Health Science Center at Houston And The University of Texas M.D.