GDF15 and Cardiac Cells: Current Concepts and New Insights
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Screening and Identification of Key Biomarkers in Clear Cell Renal Cell Carcinoma Based on Bioinformatics Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Screening and identification of key biomarkers in clear cell renal cell carcinoma based on bioinformatics analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract Clear cell renal cell carcinoma (ccRCC) is one of the most common types of malignancy of the urinary system. The pathogenesis and effective diagnosis of ccRCC have become popular topics for research in the previous decade. In the current study, an integrated bioinformatics analysis was performed to identify core genes associated in ccRCC. An expression dataset (GSE105261) was downloaded from the Gene Expression Omnibus database, and included 26 ccRCC and 9 normal kideny samples. Assessment of the microarray dataset led to the recognition of differentially expressed genes (DEGs), which was subsequently used for pathway and gene ontology (GO) enrichment analysis. -
The GDNF Family: a Role in Cancer? Graeme C
Volume 20 Number 1 January 2018 pp. 99–117 99 www.neoplasia.com The GDNF Family: A Role in Cancer? Graeme C. Fielder*, 1, 2, Teresa Wen-Shan Yang*, 1, Mahalakshmi Razdan†, Yan Li†, Jun Lu†, Jo K. Perry‡, Peter E. Lobie§ and Dong-Xu Liu† *University of Auckland, Auckland, New Zealand; †The Centre for Biomedical and Chemical Sciences, School of Science, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand; ‡Liggins Institute, University of Auckland, Auckland, New Zealand; §Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore; Tsinghua Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, Guangdong, P. R. China Abstract The glial cell line–derived neurotrophic factor (GDNF) family of ligands (GFLs) comprising of GDNF, neurturin, artemin, and persephin plays an important role in the development and maintenance of the central and peripheral nervous system, renal morphogenesis, and spermatogenesis. Here we review our current understanding of GFL biology, and supported by recent progress in the area, we examine their emerging role in endocrine-related and other non–hormone-dependent solid neoplasms. The ability of GFLs to elicit actions that resemble those perturbed in an oncogenic phenotype, alongside mounting evidence of GFL involvement in tumor progression, presents novel opportunities for therapeutic intervention. Neoplasia (2018) 20, 99–117 Introduction GFL Signaling The glial cell line–derived neurotrophic factor (GDNF) family of Each member of the GDNF family is expressed as a pre-pro-precursor ligands (GFLs) is comprised of four structurally related factors: protein, which is proteolytically cleaved at a putative furin-like GDNF,neurturin(NRTN),artemin(ARTN),andpersephin cleavage site (RAAR) by yet unidentified enzymes to generate an (PSPN) [1–3]. -
GDNF Family Ligands and DRG Sensory Neurons 4337
Development 127, 4335-4344 (2000) 4335 Printed in Great Britain © The Company of Biologists Limited 2000 DEV1547 Positive and negative interactions of GDNF, NTN and ART in developing sensory neuron subpopulations, and their collaboration with neurotrophins Christel Baudet1, Åsa Mikaels1, Heiner Westphal2, Jens Johansen3, Teit E. Johansen3 and Patrik Ernfors1,* 1Laboratory of Molecular Neurobiology, Medical Biochemistry and Biophysics, Karolinska Institutet, S-171 77 Stockholm, Sweden 2Laboratory of Mammalian Genes and Development, National Institute of Health, Bethesda, MD 20892, USA 3NsGene A/S, DK-2570 Ballerup, Denmark *Author for correspondence (e-mail: [email protected]) Accepted 25 July; published on WWW 26 September 2000 SUMMARY Glial cell line-derived neurotrophic factor (GDNF), family receptors are medium sized, whereas small-caliber neurturin (NTN) and neublastin/artemin (ART) are distant nociceptive cells preferentially express a single receptor. In members of the transforming growth factor β family, contrast to brain-derived neurotrophic factor (BDNF)- and have been shown to elicit neurotrophic effects upon dependent neurons, embryonic nerve growth factor (NGF)- several classes of peripheral and central neurons. Limited dependent nociceptive neurons switch dependency to information from in vitro and expression studies has GDNF, NTN and ART postnatally. Neurons that survive in also substantiated a role for GDNF family ligands in the presence of neurotrophin 3 (NT3) or neurotrophin 4 mammalian somatosensory neuron development. Here, we (NT4), including proprioceptive afferents, Merkel end show that although dorsal root ganglion (DRG) sensory organs and D-hair afferents, are also supported by GDNF neurons express GDNF family receptors embryonically, family ligands neonatally, although at postnatal stages they they do not survive in response to their ligands. -
Current and Future Role of Tyrosine Kinases Inhibition in Thyroid Cancer: from Biology to Therapy
International Journal of Molecular Sciences Review Current and Future Role of Tyrosine Kinases Inhibition in Thyroid Cancer: From Biology to Therapy 1, 1, 1,2,3, 3,4 María San Román Gil y, Javier Pozas y, Javier Molina-Cerrillo * , Joaquín Gómez , Héctor Pian 3,5, Miguel Pozas 1, Alfredo Carrato 1,2,3 , Enrique Grande 6 and Teresa Alonso-Gordoa 1,2,3 1 Medical Oncology Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain; [email protected] (M.S.R.G.); [email protected] (J.P.); [email protected] (M.P.); [email protected] (A.C.); [email protected] (T.A.-G.) 2 The Ramon y Cajal Health Research Institute (IRYCIS), CIBERONC, 28034 Madrid, Spain 3 Medicine School, Alcalá University, 28805 Madrid, Spain; [email protected] (J.G.); [email protected] (H.P.) 4 General Surgery Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain 5 Pathology Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain 6 Medical Oncology Department, MD Anderson Cancer Center, 28033 Madrid, Spain; [email protected] * Correspondence: [email protected] These authors have contributed equally to this work. y Received: 30 June 2020; Accepted: 10 July 2020; Published: 13 July 2020 Abstract: Thyroid cancer represents a heterogenous disease whose incidence has increased in the last decades. Although three main different subtypes have been described, molecular characterization is progressively being included in the diagnostic and therapeutic algorithm of these patients. In fact, thyroid cancer is a landmark in the oncological approach to solid tumors as it harbors key genetic alterations driving tumor progression that have been demonstrated to be potential actionable targets. -
Regulation of GDNF Expression in Sertoli Cells
157 3 REPRODUCTIONREVIEW Regulation of GDNF expression in Sertoli cells Parag A Parekh1, Thomas X Garcia2,3 and Marie-Claude Hofmann1 1Department of Endocrine Neoplasia, UT MD Anderson Cancer Center, Houston, Texas, USA, 2Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas, USA, 3Department of Biological and Environmental Sciences, University of Houston-Clear Lake, Houston, Texas, USA Correspondence should be addressed to M-C Hofmann; Email: [email protected] Abstract Sertoli cells regulate male germ cell proliferation and differentiation and are a critical component of the spermatogonial stem cell (SSC) niche, where homeostasis is maintained by the interplay of several signaling pathways and growth factors. These factors are secreted by Sertoli cells located within the seminiferous epithelium, and by interstitial cells residing between the seminiferous tubules. Sertoli cells and peritubular myoid cells produce glial cell line-derived neurotrophic factor (GDNF), which binds to the RET/GFRA1 receptor complex at the surface of undifferentiated spermatogonia. GDNF is known for its ability to drive SSC self- renewal and proliferation of their direct cell progeny. Even though the effects of GDNF are well studied, our understanding of the regulation its expression is still limited. The purpose of this review is to discuss how GDNF expression in Sertoli cells is modulated within the niche, and how these mechanisms impact germ cell homeostasis. Reproduction (2019) 157 R95–R107 Introduction reserve stem cells (A0), coexisting with a population of renewing spermatogonia that they called A1–A4 Proper regulation of stem cell fate is critical to maintain (Clermont & Leblond 1953, Clermont & Bustos-Obregon adequate cell numbers in health and diseases. -
GDF15/GFRAL Pathway As a Metabolic Signature for Cachexia In
Journal of Cancer 2021, Vol. 12 1125 Ivyspring International Publisher Journal of Cancer 2021; 12(4): 1125-1132. doi: 10.7150/jca.50376 Review GDF15/GFRAL Pathway as a Metabolic Signature for Cachexia in Patients with Cancer Darakhshan Sohail Ahmed1,2, Stéphane Isnard1,2,3, John Lin1,2, Bertrand Routy4,5, Jean-Pierre Routy1,2,6 1. Infectious Disease and Immunity in Global Health Program, Research Institute of McGill University Health Centre, Montreal, QC, Canada 2. Division of Hematology and Chronic Viral Illness Service, McGill University Health Centre, Montreal, QC, Canada 3. CIHR Canadian HIV Trials Network, Vancouver, BC 4. Division of Hémato-oncologie, Centre hospitalier de l’Université de Montréal 5. Centre de recherche du Centre hospitalier de l’Université de Montréal 6. Division of Hematology, McGill University Health Centre, Montreal, QC, Canada Corresponding author: Dr. Jean-Pierre Routy. Email: [email protected] © The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. Received: 2020.07.06; Accepted: 2020.11.06; Published: 2021.01.01 Abstract Cachexia is a metabolic mutiny that directly reduces life expectancy in chronic conditions such as cancer. The underlying mechanisms associated with cachexia involve inflammation, metabolism, and anorexia. Therefore, the need to identify cachexia biomarkers is warranted to better understand catabolism change and assess various therapeutic interventions. Among inflammatory proteins, growth differentiation factor-15 (GDF15), an atypical transforming growth factor-beta (TGF-β) superfamily member, emerges as a stress-related hormone. -
Neuronal Types and Their Specification Dynamics in the Autonomic Nervous System
From the Department of Medical Biochemistry and Biophysics Karolinska Institutet, Stockholm, Sweden NEURONAL TYPES AND THEIR SPECIFICATION DYNAMICS IN THE AUTONOMIC NERVOUS SYSTEM Alessandro Furlan Stockholm 2016 All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by E-Print AB © Alessandro Furlan, 2016 ISBN 978-91-7676-419-0 On the cover: abstract illustration of sympathetic neurons extending their axons Credits: Gioele La Manno NEURONAL TYPES AND THEIR SPECIFICATION DYNAMICS IN THE AUTONOMIC NERVOUS SYSTEM THESIS FOR DOCTORAL DEGREE (Ph.D.) By Alessandro Furlan Principal Supervisor: Opponent: Prof. Patrik Ernfors Prof. Hermann Rohrer Karolinska Institutet Max Planck Institute for Brain Research Department of Medical Biochemistry and Research Group Developmental Neurobiology Biophysics Division of Molecular Neurobiology Examination Board: Prof. Jonas Muhr Co-supervisor(s): Karolinska Institutet Prof. Ola Hermansson Department of Cell and Molecular Biology Karolinska Institutet Department of Neuroscience Prof. Tomas Hökfelt Karolinska Institutet Assistant Prof. Francois Lallemend Department of Neuroscience Karolinska Institutet Division of Chemical Neurotransmission Department of Neuroscience Prof. Ted Ebedal Uppsala University Department of Neuroscience Division of Developmental Neuroscience To my parents ABSTRACT The autonomic nervous system is formed by a sympathetic and a parasympathetic division that have complementary roles in the maintenance of body homeostasis. Autonomic neurons, also known as visceral motor neurons, are tonically active and innervate virtually every organ in our body. For instance, cardiac outflow, thermoregulation and even the focusing of our eyes are just some of the plethora of physiological functions under the control of this system. Consequently, perturbation of autonomic nervous system activity can lead to a broad spectrum of disorders collectively known as dysautonomia and other diseases such as hypertension. -
GDF11, GDF15), Eotaxin-1 (CCL11) and Junctional Adhesion Molecule a (JAM-A) in the Regulation of Blood Pressure in Women with Essential Hypertension
MOJ Gerontology & Geriatrics Research Article Open Access The role of growth differentiation factors 11 and 15 (GDF11, GDF15), eotaxin-1 (CCL11) and junctional adhesion molecule a (JAM-A) in the regulation of blood pressure in women with essential hypertension Abstract Volume 3 Issue 1 - 2018 Introduction: Evaluation of biomarkers of arterial hypertension (AH) could be Kuznik BI,1,2 Davydov SO,1,2 Stepanov AV,1,2 considered to be useful at early stages of hypertension. Guseva ES,1,2 Smolyakov YN,1 Tsybikov NN,1 Objective: We hypothesized that the levels of junctional adhesion molecule-A Magen E3 (JAM-A), eotaxin/C-C motif chemokine ligand 11 (CCL11), growth differentiation 1Chita State Medical Academy, Russia factor 11 (GDF11), and growth differentiation factor-15 (GDF15) might be a 2Innovative Clinic Health Academy, Russia biochemical markers of AH. 3Medicine C Department, Clinical Immunology and Allergy Division, Ben Gurion University of the Negev, Israel Methods: We examined the association between blood levels of these chemokines and blood pressure in middle-aged female hypertensives in three groups; 37 patients Correspondence: Eli Magen MD, Medicine C Department, treated by antihypertensive medications (T-AH) group, 16 untreated hypertensive Clinical Immunology and Allergy Division, Ben Gurion University patients (U-AH group) and 29 healthy subjects (control group). JAM-A, CCL11, of Negev, Zionut 21/33, Ashdod, 77456, Israel, GDF11, and GDF15 concentrations were evaluated with ELISA. Email [email protected] Results: The patients of T-AH group and UT-AH group were characterized by higher Received: December 01, 2017 | Published: February 09, 2018 blood levels of GDF15 (13.9±0.9 pg/ml - T-AH group and 14.6±5.9 pg/ml - UT-AH group) than normotensive control subjects (6.1±2.3 pg/dl; p<0.001). -
Multiple Endocrine Neoplasia Type 2: an Overview Jessica Moline, MS1, and Charis Eng, MD, Phd1,2,3,4
GENETEST REVIEW Genetics in Medicine Multiple endocrine neoplasia type 2: An overview Jessica Moline, MS1, and Charis Eng, MD, PhD1,2,3,4 TABLE OF CONTENTS Clinical Description of MEN 2 .......................................................................755 Surveillance...................................................................................................760 Multiple endocrine neoplasia type 2A (OMIM# 171400) ....................756 Medullary thyroid carcinoma ................................................................760 Familial medullary thyroid carcinoma (OMIM# 155240).....................756 Pheochromocytoma ................................................................................760 Multiple endocrine neoplasia type 2B (OMIM# 162300) ....................756 Parathyroid adenoma or hyperplasia ...................................................761 Diagnosis and testing......................................................................................756 Hypoparathyroidism................................................................................761 Clinical diagnosis: MEN 2A........................................................................756 Agents/circumstances to avoid .................................................................761 Clinical diagnosis: FMTC ............................................................................756 Testing of relatives at risk...........................................................................761 Clinical diagnosis: MEN 2B ........................................................................756 -
Growth/Differentiation Factor 15 Causes Tgfβ-Activated Kinase 1
Skeletal Muscle Thorax: first published as 10.1136/thoraxjnl-2017-211440 on 15 December 2018. Downloaded from ORIGINAL ARTICLE Growth/differentiation factor 15 causes TGFβ- activated kinase 1-dependent muscle atrophy in pulmonary arterial hypertension Benjamin E Garfield,1,2 Alexi Crosby,3 Dongmin Shao,1,2 Peiran Yang,3 Cai Read,3 Steven Sawiak,3 Stephen Moore,3 Lisa Parfitt,2 Carl Harries,2 Martin Rice,3 Richard Paul,4 Mark L Ormiston,5 Nicholas W Morrell,3 Michael I Polkey,4 Stephen John Wort,1,2 Paul R Kemp1 ► Additional material is ABSTRact published online only. To view Introduction Skeletal muscle dysfunction is a Key messages please visit the journal online (http:// dx. doi. org/ 10. 1136/ clinically important complication of pulmonary arterial thoraxjnl- 2017- 211440). hypertension (PAH). Growth/differentiation factor What is the key question? 15 (GDF-15), a prognostic marker in PAH, has been ► What is the association between growth/ For numbered affiliations see associated with muscle loss in other conditions. We differentiation factor 15 (GDF-15) and muscle end of article. aimed to define the associations ofG DF-15 and muscle wasting in pulmonary arterial hypertension? Correspondence to wasting in PAH, to assess its utility as a biomarker of What is the bottom line? Dr Stephen John Wort, Section muscle loss and to investigate its downstream signalling ► GDF-15 is a responsive biomarker for muscle of Vascular Biology, NHLI, pathway as a therapeutic target. wasting in pulmonary arterial hypertension Imperial College London, Methods GDF-15 levels and measures of muscle size London SW3 6PT, UK; that acts through TGFβ-activated kinase s. -
GDF15 Plasma Level Is Inversely Associated with Level of Physical Activity and Correlates with Markers of Inflammation and Muscl
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Archivio istituzionale della ricerca - Alma Mater Studiorum Università di Bologna ORIGINAL RESEARCH published: 12 May 2020 doi: 10.3389/fimmu.2020.00915 GDF15 Plasma Level Is Inversely Associated With Level of Physical Activity and Correlates With Markers of Inflammation and Muscle Weakness Maria Conte 1*†, Morena Martucci 1, Giovanni Mosconi 2, Antonio Chiariello 1, Maria Cappuccilli 1, Valentina Totti 3, Aurelia Santoro 1, Claudio Franceschi 4 and Stefano Salvioli 1 1 Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy, 2 Nephrology and Dialysis, Morgagni-Pierantoni Hospital, AUSL Romagna, Forlì, Italy, 3 Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy, 4 Laboratory of Systems Medicine of Healthy Aging and Department of Applied Mathematics, Lobachevsky University, Nizhny Novgorod, Russia Edited by: Moisés Evandro Bauer, Growth differentiation factor 15 (GDF15) is a stress molecule produced in response to Pontifical Catholic University of Rio mitochondrial, metabolic and inflammatory stress with a number of beneficial effects on Grande Do Sul, Brazil metabolism. However, at the level of skeletal muscle it is still unclear whether GDF15 is Reviewed by: Gilson Dorneles, beneficial or detrimental. The aim of the study was to analyse the levels of circulating Federal University of Health Sciences GDF15 in people of different age, characterized by different level of physical activity of Porto Alegre, Brazil Karsten Krüger, and to seek for correlation with hematological parameters related to inflammation. The Leibniz University Hannover, Germany plasma concentration of GDF15 was determined in a total of 228 subjects in the age Will Trim, range from 18 to 83 years. -
Mechanically-Induced GDF15 Secretion by Periodontal Ligament
www.nature.com/scientificreports OPEN Mechanically-induced GDF15 Secretion by Periodontal Ligament Fibroblasts Regulates Osteogenic Received: 14 March 2019 Accepted: 17 July 2019 Transcription Published: xx xx xxxx Judit Symmank 1, Sarah Zimmermann2, Jutta Goldschmitt3, Eik Schiegnitz3, Michael Wolf4, Heinrich Wehrbein2 & Collin Jacobs1 The alveolar bone provides structural support against compressive and tensile forces generated during mastication as well as during orthodontic treatment. To avoid abnormal alveolar bone resorption and tooth loss, a balanced bone turnover by bone-degrading osteoclasts and bone-generating osteoblasts is of great relevance. Unlike its contradictory role in regulating osteoclast and osteoblast cell diferentiation, the TGF-β/BMP-family member GDF15 is well known for its important functions in the regulation of cell metabolism, as well as cell fate and survival in response to cellular stress. Here, we provide frst evidence for a potential role of GDF15 in translating mechanical stimuli into cellular changes in immature osteoblasts. We detected enhanced levels of GDF15 in vivo in periodontal ligament cells after the simulation of tooth movement in rat model system as well as in vitro in mechanically stressed human periodontal ligament fbroblasts. Moreover, mechanical stimulation enhanced GDF15 secretion by periodontal ligament cells and the stimulation of human primary osteoblast with GDF15 in vitro resulted in an increased transcription of osteogenic marker genes like RUNX2, osteocalcin (OCN) and alkaline phosphatase (ALP). Together, the present data emphasize for the frst time a potential function of GDF15 in regulating diferentiation programs of immature osteoblasts according to mechanical stimulation. Te continuous remodeling of the alveolar bone in response to mechanical stimulation maintains strength, prevents tissue damage and secures teeth anchorage1.