RT² Profiler PCR Array (96-Well Format and 384-Well [4 X 96] Format)
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Altered Integrin Alpha 6 Expression As a Rescue for Muscle Fiber Detachment in Zebrafish (Danio Rerio)
The University of Maine DigitalCommons@UMaine Honors College Spring 2014 Altered Integrin Alpha 6 Expression As A Rescue For Muscle Fiber Detachment In Zebrafish (Danio Rerio) Rose E. McGlauflin Follow this and additional works at: https://digitalcommons.library.umaine.edu/honors Part of the Animal Diseases Commons, and the Musculoskeletal Diseases Commons Recommended Citation McGlauflin, Rose E., Alter" ed Integrin Alpha 6 Expression As A Rescue For Muscle Fiber Detachment In Zebrafish (Danio Rerio)" (2014). Honors College. 140. https://digitalcommons.library.umaine.edu/honors/140 This Honors Thesis is brought to you for free and open access by DigitalCommons@UMaine. It has been accepted for inclusion in Honors College by an authorized administrator of DigitalCommons@UMaine. For more information, please contact [email protected]. ALTERED INTEGRIN ALPHA 6 EXPRESSION AS A RESCUE FOR MUSCLE FIBER DETACHMENT IN ZEBRAFISH (DANIO RERIO) by Rose E. McGlauflin A Thesis Submitted in Partial Fulfillment of the Requirements for a Degree with Honors (Biology) The Honors College University of Maine May 2014 Advisory Committee: Clarissa A. Henry, Ph.D., Associate Professor of Biological Sciences, Advisor Mary S. Tyler, Ph.D., Professor of Zoology Mary Astumian, Henry Lab Manager Michelle Smith, Ph.D., Assistant Professor of Biological Sciences Mark Haggerty, Ph.D., Honors Preceptor for Civic Engagement Abstract Cells adhere to their extracellular matrix by way of integrins, transmembrane molecules that attach the cytoskeleton to the extracellular basement membrane (one kind of extracellular matrix). In some muscular dystrophies, specific integrins are disrupted and muscle fibers detach from the myotendenous junction and degenerate. This integrin disruption causes a constant cycle of regeneration and degeneration, which greatly harms the tissue over time. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Comparison of Gene Expression Profiles Between Dental Pulp and Periodontal Ligament Tissues in Humans
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 40: 647-660, 2017 Comparison of gene expression profiles between dental pulp and periodontal ligament tissues in humans AI-XIU GONG1*, JING-HAN ZHANG2*, JING LI1, JUN WU3, LIN WANG4 and DENG-SHUN MIAO3 Departments of 1Stomatology, and 2Neonatology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008; 3State Key Laboratory of Reproductive Medicine, The Research Center for Bone and Stem Cells, Department of Anatomy, Histology and Embryology, Nanjing Medical University; 4Jiangsu Key Laboratory of Oral Diseases, Department of Orthodontics, School of Stomatology, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China Received March 16, 2016; Accepted June 16, 2017 DOI: 10.3892/ijmm.2017.3065 Abstract. There are anatomical and functional differ- DP samples. The gene expression profiles provide novel insight ences between human dental pulp (DP) and periodontal into the characterization of DP and PDL tissues, and contribute ligament (PDL). However, the molecular biological differ- to our understanding of the potential molecular mechanisms of ences and function of these tissues are poorly understood. dental tissue mineralization and regeneration. In the present study, we employed a cDNA microarray array to screen for differentially expressed genes (DEGs) between Introduction human DP and PDL tissues, and used the online software WebGestalt to perform the functional analysis of the DEGs. Dental pulp (DP) tissue, termed as the ‘ectomesenchyme’, is In addition, the STRING database and KEGG pathway derived from ectodermal cells that grow on the periphery of analysis were applied for interaction network and pathway the neural tube, migrate to the oral position and then differen- analysis of the DEGs. -
Impaired Axonal Regeneration in Α7 Integrin-Deficient Mice
The Journal of Neuroscience, March 1, 2000, 20(5):1822–1830 Impaired Axonal Regeneration in ␣7 Integrin-Deficient Mice Alexander Werner,1 Michael Willem,2 Leonard L. Jones,1 Georg W. Kreutzberg,1 Ulrike Mayer,2 and Gennadij Raivich1 1Department of Neuromorphology, Max-Planck-Institute of Neurobiology, and 2Department of Protein Chemistry, Max- Planck-Institute of Biochemistry, 82152 Martinsried, Germany The interplay between growing axons and the extracellular the regenerating facial nerve. Transgenic deletion of the ␣7 substrate is pivotal for directing axonal outgrowth during de- subunit caused a significant reduction of axonal elongation. velopment and regeneration. Here we show an important role The associated delay in the reinnervation of the whiskerpad, a for the neuronal cell adhesion molecule ␣71 integrin during peripheral target of the facial motor neurons, points to an peripheral nerve regeneration. Axotomy led to a strong increase important role for this integrin in the successful execution of of this integrin on regenerating motor and sensory neurons, but axonal regeneration. not on the normally nonregenerating CNS neurons. ␣7 and 1 Key words: axonal regeneration; reinnervation; facial nerve; subunits were present on the axons and their growth cones in growth cone; motoneuron; integrin; knock-out mice Changes in adhesion properties of transected axons and their Flier et al., 1995; Kil and Bronner-Fraser, 1996; Velling et al., environment are essential for regeneration. In the proximal part, 1996). In the adult nervous system, we now show that ␣7is the tips of the transected axons transform into growth cones that strongly upregulated in axotomized neurons in various injury home onto the distal part of the nerve and enter the endoneurial models during peripheral nerve regeneration, but not after CNS tubes on their way toward the denervated tissue (Fawcett, 1992; injury. -
Biomimetic Surfaces for Cell Engineering
Chapter 18 Biomimetic Surfaces for Cell Engineering John H. Slater, Omar A. Banda, Keely A. Heintz and Hetty T. Nie Cell behavior, in particular, migration, proliferation, differentiation, apoptosis, and activation, is mediated by a multitude of environmental factors: (i) extracellular matrix (ECM) properties including molecular composition, ligand density, ligand gradients, stiffness, topography, and degradability; (ii) soluble factors including type, concentration, and gradients; (iii) cell–cell interactions; and (iv) external forc- es such as shear stress, material strain, osmotic pressure, and temperature changes (Fig. 18.1). The coordinated influence of these environmental cues regulate em- bryonic development, tissue function, homeostasis, and wound healing as well as other crucial events in vivo [1–3]. From a fundamental biology perspective, it is of great interest to understand how these environmental factors regulate cell fate and ultimately cell and tissue function. From an engineering perspective, it is of interest to determine how to present these factors in a well-controlled manner to elicit a de- sired cell output for cell and tissue engineering applications. Both biophysical and biochemical factors mediate intracellular signaling cascades that influence gene ex- pression and ultimately cell behavior [4–7], making it difficult to unravel the hierar- chy of cell fate stimuli [8]. Accordingly, much effort has focused on the fabrication of biomimetic surfaces that recapitulate a single or many aspects of the in vivo mi- croenvironment including topography [9–12], elasticity [5], and ligand presentation [13–17], and by structured materials that allow for control over cell shape [18–23], spreading [18, 23–25], and cytoskeletal tension [26–28]. -
(ITGA7) Gene Integrin; ITGA7; PCR; Myopathy Keywords: Species: Homo Sapiens Change Is: Polymorphism
HUMAN MUTATION Mutation and Polymorphism Report #141 (2000) Online Mutation and Polymorphism Report Authors: Doroti Pirulli 1, Silvia Zezlina 1 , Laura Vatta 1, Paola Di Stefano 2 , Michele Boniotto 1, Guido Tarone 2, Tiziana Mongini 3, Isabella Ugo 3, Laura Palmucci 3, Antonio Amoroso 1, and Sergio Crovella 1 Affiliations 1 Medical Genetic Service, IRCCS Burlo Garofolo, Chair of Genetics, University of Trieste, Italy; 2 Department of Genetics, Biology and Biochemistry, University of Turin, Italy; 3 Department of Neuroscience, University of Turin, Italy Corresponding Author Address and E-mail: Sergio Crovella, Chair of Genetics, University of Trieste, Medical Genetic Service, IRCCS Burlo Garofolo,Via dell'Istria 65/1,34137 Trieste, Italy; E-mail: [email protected] Title : A new polymorphism, g119A>G, in the integrin alpha 7 (ITGA7) gene integrin; ITGA7; PCR; myopathy Keywords: Species: Homo sapiens Change is: Polymorphism Gene/Locus Name: integrin, alpha 7 Symbol: ITGA7 Genbank accession number: AJ228850 exon 15 OMIM accession number: 600536 Locus specific database: Chromosomal location: 12q13 Inheritance: Unknown Mutation / polymorphism name Nucleotide change–Systematic name: g119A>G Amino acid change–Trivial name: H651R Mutation / polymorphism type: Missense Polymorphism frequency: 44/56 G/A Detection method: RFLP-PCR, Direct sequencing Detection conditions: RT-PCR Primers F: 5'-TCAAGAGCTTCGGCTACTCC-3' R: 5'-AGTCAGGAAGCATGACCAGG-3' Genomic PCR-Primers F: 5'-GCCCCCTGCCTTGCC-3' R: 5'-AGGGCTTTCTCTCAATCCTTGA-3' RT-PCR conditions RT-PCR was performed on total mRNA of 3 unclassified myopathy patients with the RNA-PCR Core Kit (PE Biosystems, Foster City, CA) HUMAN MUTATION Mutation and Polymorphism Report #141 (2000) Online using the reverse primer as antisense. -
Integrin Alpha-5 Silencing Leads to Myofibroblastic Differentiation In
TAJ0010.1177/2040622320936023Therapeutic Advances in Chronic DiseaseGE Shochet 936023research-article20202020 Therapeutic Advances in Chronic Disease Original Article Ther Adv Chronic Dis Integrin alpha-5 silencing leads to 2020, Vol. 11: 1–12 DOI:https://doi.org/10.1177/2040622320936023 10.1177/ myofibroblastic differentiation in IPF- 2040622320936023https://doi.org/10.1177/2040622320936023 © The Author(s), 2020. Article reuse guidelines: derived human lung fibroblasts sagepub.com/journals- permissions Gali Epstein Shochet* , Elizabetha Brook*, Becky Bardenstein-Wald, Hanna Grobe, Evgeny Edelstein, Lilach Israeli-Shani and David Shitrit Abstract Background and objective: The term ‘fibroblast’ covers a heterogeneous cell population in idiopathic pulmonary fibrosis (IPF). The fibroblasts are considered as main effector cells, because they promote disease progression by releasing exaggerated amounts of extracellular matrix proteins and modifying cell microenvironment. As IPF-derived human lung fibroblasts (IPF-HLFs) were shown to express higher levels of integrin alpha-5 (ITGA5) than normal derived HLFs (N-HLFs), we explored the importance of ITGA5 to IPF progression. Methods: IPF-HLF and N-HLF primary cultures were established. ITGA5 was silenced by specific small interfering RNA (siRNA)s and its effects on cell phenotype (e.g. cell number, size, cell death, migration) and gene expression (e.g. RNA sequencing, quantitative polymerase chain reaction [qPCR], western blot and immunofluorescence) were tested. Specific integrin expression was evaluated in IPF patient formalin-fixed paraffin embedded sections by immunohistochemistry (IHC). Results: ITGA5-silencing resulted in reduced IPF-HLF proliferation rates and cell migration (p < 0.05), as well as elevated cell death. transforming growth factor beta (TGF-β) targets (e.g. Fibronectin (FN1), Matrix metalloproteinase 2 (MMP2), TGFB1) were surprisingly elevated following ITGA5 silencing (p < 0.05). -
Development of Novel Strategies to Improve Skeletal Muscle Repair and Adaptation Following Eccentric Exercise
DEVELOPMENT OF NOVEL STRATEGIES TO IMPROVE SKELETAL MUSCLE REPAIR AND ADAPTATION FOLLOWING ECCENTRIC EXERCISE BY KAI ZOU DISSERTATION Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Kinesiology in the Graduate College of the University of Illinois at Urbana-Champaign, 2014 Urbana, Illinois Doctoral Committee: Assistant Professor Marni D. Boppart, Chair Associate Professor Kenneth R. Wilund Professor Jeffrey A. Woods Professor Jie Chen ABSTRACT Eccentric contractions, often required for participation in resistance training, as well as daily activities, can injure skeletal muscle. The repair of muscle damage is essential for effective remodeling, tissue maintenance, and initiation of beneficial adaptations post-exercise. We have previously demonstrated that transgenic overexpression of the α7BX2 integrin in skeletal muscle (MCK: α7BX2; α7Tg) enhances muscle repair and the adaptive response following eccentric exercise. Recent studies have provided evidence that mesenchymal stem cells residing in skeletal muscle (mMSCs) contribute to repair following injury by secreting a variety of factors that are important for progenitor cell (satellite cell) activation. Our lab has also previously established that mMSC proliferation and quantity is increased following eccentric exercise in a manner dependent on the presence of the α7BX2 integrin. Preliminary cell culture experiments conducted in our lab suggest that mMSC paracrine factor gene expression is enhanced in the presence of laminin, an important component of the basal lamina that provides the microenvironment for muscle stem cells. Thus, the purpose of this study was to determine the extent to which mMSC and laminin-111 (LM-111) supplementation can enhance muscle repair and/or the adaptive response associated with eccentric exercise. -
Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy*□S
crossmark Research Author’s Choice © 2016 by The American Society for Biochemistry and Molecular Biology, Inc. This paper is available on line at http://www.mcponline.org Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy*□S Rolf Turk‡§¶ʈ**, Jordy J. Hsiao¶, Melinda M. Smits¶, Brandon H. Ng¶, Tyler C. Pospisil‡§¶ʈ**, Kayla S. Jones‡§¶ʈ**, Kevin P. Campbell‡§¶ʈ**, and Michael E. Wright¶‡‡ Mutations in genes encoding components of the sar- The muscular dystrophies are hereditary diseases charac- colemmal dystrophin-glycoprotein complex (DGC) are re- terized primarily by the progressive degeneration and weak- sponsible for a large number of muscular dystrophies. As ness of skeletal muscle. Most are caused by deficiencies in such, molecular dissection of the DGC is expected to both proteins associated with the cell membrane (i.e. the sarco- reveal pathological mechanisms, and provides a biologi- lemma in skeletal muscle), and typical features include insta- cal framework for validating new DGC components. Es- bility of the sarcolemma and consequent death of the myofi- tablishment of the molecular composition of plasma- ber (1). membrane protein complexes has been hampered by a One class of muscular dystrophies is caused by mutations lack of suitable biochemical approaches. Here we present in genes that encode components of the sarcolemmal dys- an analytical workflow based upon the principles of pro- tein correlation profiling that has enabled us to model the trophin-glycoprotein complex (DGC). In differentiated skeletal molecular composition of the DGC in mouse skeletal mus- muscle, this structure links the extracellular matrix to the cle. We also report our analysis of protein complexes in intracellular cytoskeleton. -
Blueprint Genetics Comprehensive Muscular Dystrophy / Myopathy Panel
Comprehensive Muscular Dystrophy / Myopathy Panel Test code: NE0701 Is a 125 gene panel that includes assessment of non-coding variants. In addition, it also includes the maternally inherited mitochondrial genome. Is ideal for patients with distal myopathy or a clinical suspicion of muscular dystrophy. Includes the smaller Nemaline Myopathy Panel, LGMD and Congenital Muscular Dystrophy Panel, Emery-Dreifuss Muscular Dystrophy Panel and Collagen Type VI-Related Disorders Panel. About Comprehensive Muscular Dystrophy / Myopathy Muscular dystrophies and myopathies are a complex group of neuromuscular or musculoskeletal disorders that typically result in progressive muscle weakness. The age of onset, affected muscle groups and additional symptoms depend on the type of the disease. Limb girdle muscular dystrophy (LGMD) is a group of disorders with atrophy and weakness of proximal limb girdle muscles, typically sparing the heart and bulbar muscles. However, cardiac and respiratory impairment may be observed in certain forms of LGMD. In congenital muscular dystrophy (CMD), the onset of muscle weakness typically presents in the newborn period or early infancy. Clinical severity, age of onset, and disease progression are highly variable among the different forms of LGMD/CMD. Phenotypes overlap both within CMD subtypes and among the congenital muscular dystrophies, congenital myopathies, and LGMDs. Emery-Dreifuss muscular dystrophy (EDMD) is a condition that affects mainly skeletal muscle and heart. Usually it presents in early childhood with contractures, which restrict the movement of certain joints – most often elbows, ankles, and neck. Most patients also experience slowly progressive muscle weakness and wasting, beginning with the upper arm and lower leg muscles and progressing to shoulders and hips. -
Fibroblasts from the Human Skin Dermo-Hypodermal Junction Are
cells Article Fibroblasts from the Human Skin Dermo-Hypodermal Junction are Distinct from Dermal Papillary and Reticular Fibroblasts and from Mesenchymal Stem Cells and Exhibit a Specific Molecular Profile Related to Extracellular Matrix Organization and Modeling Valérie Haydont 1,*, Véronique Neiveyans 1, Philippe Perez 1, Élodie Busson 2, 2 1, 3,4,5,6, , Jean-Jacques Lataillade , Daniel Asselineau y and Nicolas O. Fortunel y * 1 Advanced Research, L’Oréal Research and Innovation, 93600 Aulnay-sous-Bois, France; [email protected] (V.N.); [email protected] (P.P.); [email protected] (D.A.) 2 Department of Medical and Surgical Assistance to the Armed Forces, French Forces Biomedical Research Institute (IRBA), 91223 CEDEX Brétigny sur Orge, France; [email protected] (É.B.); [email protected] (J.-J.L.) 3 Laboratoire de Génomique et Radiobiologie de la Kératinopoïèse, Institut de Biologie François Jacob, CEA/DRF/IRCM, 91000 Evry, France 4 INSERM U967, 92260 Fontenay-aux-Roses, France 5 Université Paris-Diderot, 75013 Paris 7, France 6 Université Paris-Saclay, 78140 Paris 11, France * Correspondence: [email protected] (V.H.); [email protected] (N.O.F.); Tel.: +33-1-48-68-96-00 (V.H.); +33-1-60-87-34-92 or +33-1-60-87-34-98 (N.O.F.) These authors contributed equally to the work. y Received: 15 December 2019; Accepted: 24 January 2020; Published: 5 February 2020 Abstract: Human skin dermis contains fibroblast subpopulations in which characterization is crucial due to their roles in extracellular matrix (ECM) biology. -
Integrin and Gene Network Analysis Reveals That ITGA5 and ITGB1 Are Prognostic in Non-Small-Cell Lung Cancer
Journal name: OncoTargets and Therapy Article Designation: Original Research Year: 2016 Volume: 9 OncoTargets and Therapy Dovepress Running head verso: Zheng et al Running head recto: ITGA5 and ITGB1 are prognostic in NSCLC open access to scientific and medical research DOI: http://dx.doi.org/10.2147/OTT.S91796 Open Access Full Text Article ORIGINAL RESEARCH Integrin and gene network analysis reveals that ITGA5 and ITGB1 are prognostic in non-small-cell lung cancer Weiqi Zheng Background: Integrin expression has been identified as a prognostic factor in non-small-cell Caihui Jiang lung cancer (NSCLC). This study was aimed at determining the predictive ability of integrins Ruifeng Li and associated genes identified within the molecular network. Patients and methods: A total of 959 patients with NSCLC from The Cancer Genome Atlas Department of Radiation Oncology, Guangqian Hospital, Quanzhou, Fujian, cohorts were enrolled in this study. The expression profile of integrins and related genes were People’s Republic of China obtained from The Cancer Genome Atlas RNAseq database. Clinicopathological characteristics, including age, sex, smoking history, stage, histological subtype, neoadjuvant therapy, radiation therapy, and overall survival (OS), were collected. Cox proportional hazards regression models as well as Kaplan–Meier curves were used to assess the relative factors. Results: In the univariate Cox regression model, ITGA1, ITGA5, ITGA6, ITGB1, ITGB4, and ITGA11 were predictive of NSCLC prognosis. After adjusting for clinical factors, ITGA5 (odds ratio =1.17, 95% confidence interval: 1.05–1.31) andITGB1 (odds ratio =1.31, 95% confidence interval: 1.10–1.55) remained statistically significant. In the gene cluster network analysis, PLAUR, ILK, SPP1, PXN, and CD9, all associated with ITGA5 and ITGB1, were identified as independent predictive factors of OS in NSCLC.