Phenotypic Modulation of Smooth Muscle Cells in Atherosclerosis Is Associated with Downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM
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Supplemental Material Table of Contents
Supplemental material Table of Contents Detailed Materials and Methods ......................................................................................................... 2 Perioperative period ........................................................................................................................... 2 Ethical aspects ................................................................................................................................... 4 Evaluation of heart failure ................................................................................................................. 4 Sample preparation for ANP mRNA expression .................................................................................. 5 Sample preparation for validative qRT-PCR (Postn, Myh7, Gpx3, Tgm2) ............................................ 6 Tissue fibrosis .................................................................................................................................... 7 Ventricular remodeling and histological tissue preservation ................................................................ 8 Evaluation of the histological preservation of cardiac tissue ................................................................ 9 Sample preparation and quantitative label-free proteomics analyses .................................................. 10 Statistical methods ........................................................................................................................... 12 References ........................................................................................................................................ -
Mechanical Forces Induce an Asthma Gene Signature in Healthy Airway Epithelial Cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T
www.nature.com/scientificreports OPEN Mechanical forces induce an asthma gene signature in healthy airway epithelial cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T. Kho4, Kelan Tantisira1, Marc Santolini 1,5, Feixiong Cheng6,7,8, Jennifer A. Mitchel3, Maureen McGill3, Michael J. O’Sullivan3, Margherita De Marzio1,3, Amitabh Sharma1, Scott H. Randell9, Jefrey M. Drazen3, Jefrey J. Fredberg3 & Scott T. Weiss1,3* Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufcient to induce infammatory, late repair, and fbrotic pathways. Remarkably, this molecular profle of non-asthmatic cells after compression recapitulated the profle of asthmatic cells before compression. Together, these results show that even in the absence of any infammatory stimulus, mechanical compression alone is sufcient to induce an asthma-like molecular signature. Bronchial epithelial cells (BECs) form a physical barrier that protects pulmonary airways from inhaled irritants and invading pathogens1,2. Moreover, environmental stimuli such as allergens, pollutants and viruses can induce constriction of the airways3 and thereby expose the bronchial epithelium to compressive mechanical stress. In BECs, this compressive stress induces structural, biophysical, as well as molecular changes4,5, that interact with nearby mesenchyme6 to cause epithelial layer unjamming1, shedding of soluble factors, production of matrix proteins, and activation matrix modifying enzymes, which then act to coordinate infammatory and remodeling processes4,7–10. -
Clinical and Prognostic Significance of MYH11 in Lung Cancer
ONCOLOGY LETTERS 19: 3899-3906, 2020 Clinical and prognostic significance ofMYH11 in lung cancer MENG-JUN NIE1,2, XIAO-TING PAN1,2, HE-YUN TAO1,2, MENG-JUN XU1,2, SHEN-LIN LIU1, WEI SUN1, JIAN WU1 and XI ZOU1 1Oncology Department, The Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu 210029; 2No.1 Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China Received May 14, 2019; Accepted February 21, 2020 DOI: 10.3892/ol.2020.11478 Abstract. Myosin heavy chain 11 (MYH11), encoded by 5-year survival rate is estimated to approximately 18% (2). the MYH11 gene, is a protein that participates in muscle Therefore, novel targets for drug treatment and prognosis of contraction through the hydrolysis of adenosine triphosphate. lung cancer are needed. Although previous studies have demonstrated that MYH11 Myosin heavy chain 11 (MYH11), which is encoded by gene expression levels are downregulated in several types of the MYH11 gene, is a smooth muscle myosin belonging to the cancer, its expression levels have rarely been investigated in myosin heavy chain family (3). MYH11 is a contractile protein lung cancer. The present study aimed to explore the clinical that slides past actin filaments to induce muscle contraction significance and prognostic value of MYH11 expression levels via adenosine triphosphate hydrolysis (4,5). Previous findings in lung cancer and to further study the underlying molecular have shown that in aortic tissue, destruction of MYH11 can mechanisms of the function of this gene. The Oncomine lead to vascular smooth muscle cell loss, disorganization database showed that the MYH11 expression levels were and hyperplasia, which is one of the mechanisms leading to decreased in lung cancer compared with those noted in the thoracic aortic aneurysms and dissections (6,7). -
Communication Pathways in Human Nonmuscle Myosin-2C 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Authors: 25 Krishna Chinthalapudia,B,C,1, Sarah M
1 Mechanistic Insights into the Active Site and Allosteric 2 Communication Pathways in Human Nonmuscle Myosin-2C 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Authors: 25 Krishna Chinthalapudia,b,c,1, Sarah M. Heisslera,d,1, Matthias Prellera,e, James R. Sellersd,2, and 26 Dietmar J. Mansteina,b,2 27 28 Author Affiliations 29 aInstitute for Biophysical Chemistry, OE4350 Hannover Medical School, 30625 Hannover, 30 Germany. 31 bDivision for Structural Biochemistry, OE8830, Hannover Medical School, 30625 Hannover, 32 Germany. 33 cCell Adhesion Laboratory, Department of Integrative Structural and Computational Biology, The 34 Scripps Research Institute, Jupiter, Florida 33458, USA. 35 dLaboratory of Molecular Physiology, NHLBI, National Institutes of Health, Bethesda, Maryland 36 20892, USA. 37 eCentre for Structural Systems Biology (CSSB), German Electron Synchrotron (DESY), 22607 38 Hamburg, Germany. 39 1K.C. and S.M.H. contributed equally to this work 40 2To whom correspondence may be addressed: E-mail: [email protected] or 41 [email protected] 42 43 1 44 Abstract 45 Despite a generic, highly conserved motor domain, ATP turnover kinetics and their activation by 46 F-actin vary greatly between myosin-2 isoforms. Here, we present a 2.25 Å crystal pre- 47 powerstroke state (ADPVO4) structure of the human nonmuscle myosin-2C motor domain, one 48 of the slowest myosins characterized. In combination with integrated mutagenesis, ensemble- 49 solution kinetics, and molecular dynamics simulation approaches, the structure reveals an 50 allosteric communication pathway that connects the distal end of the motor domain with the 51 active site. -
Integrating Single-Step GWAS and Bipartite Networks Reconstruction Provides Novel Insights Into Yearling Weight and Carcass Traits in Hanwoo Beef Cattle
animals Article Integrating Single-Step GWAS and Bipartite Networks Reconstruction Provides Novel Insights into Yearling Weight and Carcass Traits in Hanwoo Beef Cattle Masoumeh Naserkheil 1 , Abolfazl Bahrami 1 , Deukhwan Lee 2,* and Hossein Mehrban 3 1 Department of Animal Science, University College of Agriculture and Natural Resources, University of Tehran, Karaj 77871-31587, Iran; [email protected] (M.N.); [email protected] (A.B.) 2 Department of Animal Life and Environment Sciences, Hankyong National University, Jungang-ro 327, Anseong-si, Gyeonggi-do 17579, Korea 3 Department of Animal Science, Shahrekord University, Shahrekord 88186-34141, Iran; [email protected] * Correspondence: [email protected]; Tel.: +82-31-670-5091 Received: 25 August 2020; Accepted: 6 October 2020; Published: 9 October 2020 Simple Summary: Hanwoo is an indigenous cattle breed in Korea and popular for meat production owing to its rapid growth and high-quality meat. Its yearling weight and carcass traits (backfat thickness, carcass weight, eye muscle area, and marbling score) are economically important for the selection of young and proven bulls. In recent decades, the advent of high throughput genotyping technologies has made it possible to perform genome-wide association studies (GWAS) for the detection of genomic regions associated with traits of economic interest in different species. In this study, we conducted a weighted single-step genome-wide association study which combines all genotypes, phenotypes and pedigree data in one step (ssGBLUP). It allows for the use of all SNPs simultaneously along with all phenotypes from genotyped and ungenotyped animals. Our results revealed 33 relevant genomic regions related to the traits of interest. -
Phenotypic Modulation of Smooth Muscle Cells in Atherosclerosis Is Associated with Downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM
Markers of smooth muscle cells Perisic et al. Phenotypic modulation of smooth muscle cells in atherosclerosis is associated with downregulation of LMOD1, SYNPO2, PDLIM7, PLN and SYNM Perisic L1, Rykaczewska U1, Razuvaev A1, Sabater-Lleal M2, Lengquist M1, Miller CL3, Ericsson I1, Röhl S1, Kronqvist M1, Aldi S1, Magné J2, Vesterlund M4, Li Y2, Yin H2, Gonzalez Diez M2, Roy J1, Baldassarre D5,6, Veglia F6, Humphries SE7, de Faire U8,9, Tremoli E5,6, on behalf of the IMPROVE study group, Odeberg J10, Vukojević V11, Lehtiö J4, Maegdefessel L2, Ehrenborg E2, Paulsson-Berne G2, Hansson GK2, Lindeman JHN12, Eriksson P2, Quertermous T3, Hamsten A2, Hedin U1 1Department of Molecular Medicine and Surgery, Karolinska Institutet, Sweden, 2Department of Medicine, Karolinska Institutet, Sweden, 3Division of Vascular Surgery, Stanford University, USA, 4Science for Life Laboratory, Sweden, 5Dipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano, Milan, Italy, 6Centro Cardiologico Monzino, IRCCS, Milan, Italy, 7British Heart Foundation Laboratories, University College of London, Department of Medicine, Rayne Building, London, United Kingdom, 8Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, 9Department of Cardiology, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden, 10Science for Life Laboratory, Department of Proteomics, Sweden, 11Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Sweden, 12Department of Vascular -
Original Article Prognostic Value of the PDLIM Family in Acute Myeloid Leukemia
Am J Transl Res 2019;11(9):6124-6131 www.ajtr.org /ISSN:1943-8141/AJTR0096980 Original Article Prognostic value of the PDLIM family in acute myeloid leukemia Longzhen Cui1,2,3,4*, Zhiheng Cheng5*, Kai Hu6*, Yifan Pang7, Yan Liu3, Tingting Qian1,2, Liang Quan1,2, Yifeng Dai8, Ying Pang1, Xu Ye1, Jinlong Shi9, Lin Fu1,2,4 1Department of Hematology, 2Translational Medicine Center, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, Guangdong, China; 3Translational Medicine Center, 4Department of Hematology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan, China; 5Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands; 6Department of Hematology and Lymphoma Research Center, Peking University, Third Hospital, Beijing 100191, China; 7Department of Medicine, William Beaumont Hospital, Royal Oak, MI 48073, USA; 8Immunoendocrinology, Division of Medical Biology, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands; 9Department of Medical Big Data, Chinese PLA General Hospital, Beijing 100853, China. *Equal contributors. Received April 22, 2019; Accepted June 26, 2019; Epub September 15, 2019; Published September 30, 2019 Abstract: Acute myeloid leukemia (AML) is a genetically complex, highly aggressive hematological malignancy. Prognosis is usually with grim. PDZ and LIM domain proteins (PDLIM) are involved in the regulation of a variety of biological processes, including cytoskeletal organization, cell differentiation, organ development, neural signaling or tumorigenesis. The clinical and prognostic value of the PDLIM family in AML is unclear. To understand the role of PDLIM expression in AML, The Cancer Genome Atlas (TCGA) database was screened and 155 de novo AML pa- tients with complete clinical information and the expression data of the PDLIM family were included in the study. -
The Transcriptomic Landscape of Prostate Cancer Development and Progression: an Integrative Analysis
cancers Article The Transcriptomic Landscape of Prostate Cancer Development and Progression: An Integrative Analysis Jacek Marzec 1,† , Helen Ross-Adams 1,*,† , Stefano Pirrò 1 , Jun Wang 1 , Yanan Zhu 2, Xueying Mao 2, Emanuela Gadaleta 1 , Amar S. Ahmad 3, Bernard V. North 3, Solène-Florence Kammerer-Jacquet 2, Elzbieta Stankiewicz 2, Sakunthala C. Kudahetti 2, Luis Beltran 4, Guoping Ren 5, Daniel M. Berney 2,4, Yong-Jie Lu 2 and Claude Chelala 1,6,* 1 Bioinformatics Unit, Centre for Cancer Biomarkers and Biotherapeutics, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, UK; [email protected] (J.M.); [email protected] (S.P.); [email protected] (J.W.); [email protected] (E.G.) 2 Centre for Cancer Biomarkers and Biotherapeutics, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, UK; [email protected] (Y.Z.); [email protected] (X.M.); solenefl[email protected] (S.-F.K.-J.); [email protected] (E.S.); [email protected] (S.C.K.); [email protected] (D.M.B.); [email protected] (Y.-J.L.) 3 Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Barts and the London School of Medicine, Queen Mary University of London, London EC1M 6BQ, UK; [email protected] (A.S.A.); [email protected] (B.V.N.) 4 Department of Pathology, Barts Health NHS, London E1 F1R, UK; [email protected] 5 Department of Pathology, The First Affiliated Hospital, Zhejiang University Medical College, Hangzhou 310058, China; [email protected] 6 Centre for Computational Biology, Life Sciences Initiative, Queen Mary University London, London EC1M 6BQ, UK * Correspondence: [email protected] (H.R.-A.); [email protected] (C.C.) † These authors contributed equally to this work. -
Cardiogenetics Testing Reference Guide December 2018
Cardiogenetics Testing reference guide December 2018 Why Choose Ambry More than 1 in 200 people have an inherited cardiovascular condition. Ambry’s mission is to provide the most advanced genetic testing information available to help you identity those at-risk and determine the best treatment options. If we know a patient has a disease-causing genetic change, not only does it mean better disease management, it also indicates that we can test others in the family and provide them with potentially life-saving information. Diseases and Testing Options cardiomyopathies arrhythmias Hypertrophic Cardiomyopathy (HCMNext) Catecholaminergic Polymorphic Ventricular Dilated Cardiomyopathy (DCMNext) Tachycardia (CPVTNext) Arrhythmogenic Right Ventricular Long QT Syndrome, Short QT Syndrome, Cardiomyopathy (ARVCNext) Brugada Syndrome (LongQTNext, RhythmNext) Cardiomyopathies (CMNext, CardioNext) Arrhythmias (RhythmNext, CardioNext) other cardio conditions Transthyretin Amyloidosis (TTR) familial hypercholesterolemia Noonan Syndrome (NoonanNext) and lipid disorders Hereditary Hemorrhagic Telangiectasia Familial Hypercholesterolemia (FHNext) (HHTNext) Sitosterolemia (Sitosterolemia Panel) Comprehensive Lipid Menu thoracic aortic aneurysms (CustomNext-Cardio) and dissections Familial Chylomicronemia Syndrome (FCSNext) Thoracic Aneurysms and Dissections, aortopathies (TAADNext) Marfan Syndrome (TAADNext) Ehlers-Danlos Syndrome (TAADNext) Targeted Panels Gene Comparison ALL PANELS HAVE A TURNAROUND TIME OF 2-3 WEEKS arrhythmias CPVTNext CPVTNext CASQ2, -
Microrna Regulatory Pathways in the Control of the Actin–Myosin Cytoskeleton
cells Review MicroRNA Regulatory Pathways in the Control of the Actin–Myosin Cytoskeleton , , Karen Uray * y , Evelin Major and Beata Lontay * y Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary; [email protected] * Correspondence: [email protected] (K.U.); [email protected] (B.L.); Tel.: +36-52-412345 (K.U. & B.L.) The authors contributed equally to the manuscript. y Received: 11 June 2020; Accepted: 7 July 2020; Published: 9 July 2020 Abstract: MicroRNAs (miRNAs) are key modulators of post-transcriptional gene regulation in a plethora of processes, including actin–myosin cytoskeleton dynamics. Recent evidence points to the widespread effects of miRNAs on actin–myosin cytoskeleton dynamics, either directly on the expression of actin and myosin genes or indirectly on the diverse signaling cascades modulating cytoskeletal arrangement. Furthermore, studies from various human models indicate that miRNAs contribute to the development of various human disorders. The potentially huge impact of miRNA-based mechanisms on cytoskeletal elements is just starting to be recognized. In this review, we summarize recent knowledge about the importance of microRNA modulation of the actin–myosin cytoskeleton affecting physiological processes, including cardiovascular function, hematopoiesis, podocyte physiology, and osteogenesis. Keywords: miRNA; actin; myosin; actin–myosin complex; Rho kinase; cancer; smooth muscle; hematopoiesis; stress fiber; gene expression; cardiovascular system; striated muscle; muscle cell differentiation; therapy 1. Introduction Actin–myosin interactions are the primary source of force generation in mammalian cells. Actin forms a cytoskeletal network and the myosin motor proteins pull actin filaments to produce contractile force. All eukaryotic cells contain an actin–myosin network inferring contractile properties to these cells. -
PDLIM7 (NM 005451) Human Untagged Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for SC111943 PDLIM7 (NM_005451) Human Untagged Clone Product data: Product Type: Expression Plasmids Product Name: PDLIM7 (NM_005451) Human Untagged Clone Tag: Tag Free Symbol: PDLIM7 Synonyms: LMP1; LMP3 Vector: pCMV6-XL4 E. coli Selection: Ampicillin (100 ug/mL) Cell Selection: None Fully Sequenced ORF: >NCBI ORF sequence for NM_005451, the custom clone sequence may differ by one or more nucleotides ATGGATTCCTTCAAAGTAGTGCTGGAGGGGCCAGCACCTTGGGGCTTCCGGCTGCAAGGGGGCAAGGACT TCAATGTGCCCCTCTCCATTTCCCGGCTCACTCCTGGGGGCAAAGCGGCGCAGGCCGGAGTGGCCGTGGG TGACTGGGTGCTGAGCATCGATGGCGAGAATGCGGGTAGCCTCACACACATCGAAGCTCAGAACAAGATC CGGGCCTGCGGGGAGCGCCTCAGCCTGGGCCTCAGCAGGGCCCAGCCGGTTCAGAGCAAACCGCAGAAGG CCTCCGCCCCCGCCGCGGACCCTCCGCGGTACACCTTTGCACCCAGCGTCTCCCTCAACAAGACGGCCCG GCCCTTTGGGGCGCCCCCGCCCGCTGACAGCGCCCCGCAGCAGAATGGACAGCCGCTCCGACCGCTGGTC CCAGATGCCAGCAAGCAGCGGCTGATGGAGAACACAGAGGACTGGCGGCCGCGGCCGGGGACAGGCCAGT CGCGTTCCTTCCGCATCCTTGCCCACCTCACAGGCACCGAGTTCATGCAAGACCCGGATGAGGAGCACCT GAAGAAATCAAGCCAGGTGCCCAGGACAGAAGCCCCAGCCCCAGCCTCATCTACACCCCAGGAGCCCTGG CCTGGCCCTACCGCCCCCAGCCCTACCAGCCGCCCGCCCTGGGCTGTGGACCCTGCGTTTGCCGAGCGCT ATGCCCCGGACAAAACGAGCACAGTGCTGACCCGGCACAGCCAGCCGGCCACGCCCACGCCGCTGCAGAG CCGCACCTCCATTGTGCAGGCAGCTGCCGGAGGGGTGCCAGGAGGGGGCAGCAACAACGGCAAGACTCCC GTGTGTCACCAGTGCCACAAGGTCATCCGGGGCCGCTACCTGGTGGCGCTGGGCCACGCGTACCACCCGG AGGAGTTTGTGTGTAGCCAGTGTGGGAAGGTCCTGGAAGAGGGTGGCTTCTTTGAGGAGAAGGGCGCCAT -
Phenotypic Variability in Familial Amyloid Polyneuropathy: TTR Modifiers in Caenorhabditis Elegans and D.ICBAS 2019 Human Models
and Human Human and Caenorhabditis Elegans DOUTORAMENTO CIÊNCIAS BIOMÉDICAS Phenotypic Variability in Familial TTR modifiers Polyneuropathy: Amyloid in Models. FerreiraMiguel Alves D 2019 Miguel Alves Ferreira. Phenotypic Variability in Familial Amyloid Polyneuropathy: TTR modifiers in Caenorhabditis Elegans and D.ICBAS 2019 Human Models. Phenotypic Variability in Familial Amyloid Polyneuropathy: TTR modifiers in Caenorhabditis Elegans and Human Models. Miguel Alves Ferreira INSTITUTO DE CIÊNCIAS BIOMÉDICAS ABEL SALAZAR D 2019 PHENOTYPIC VARIABILITY IN FAMILIAL AMYLOID POLYNEUROPATHY: TTR MODIFIERS IN CAENORHABDITIS ELEGANS AND HUMAN MODELS. Doctoral program in Biomedical Sciences MIGUEL FERNANDO ALVES FERREIRA PHENOTYPIC VARIABILITY IN FAMILIAL AMYLOID POLYNEUROPATHY: TTR MODIFIERS IN CAENORHABDITIS ELEGANS AND HUMAN MODELS. Tese de Candidatura ao grau de Doutor em Ciências Biomédicas submetida ao Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto. Orientador – Prof. Doutora Carolina Luísa Cardoso Lemos Categoria – Professora Auxiliar Convidada Afiliação – Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto. Co-orientadora – Prof. Doutora Alda Maria Botelho Correia de Sousa Categoria – Professora Associada com Agregação Afiliação – Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto. Co-orientadora – Prof. Doutora Sandra Encalada Categoria – Assistant Professor Afiliação – The Scripps Research Institute (TSRI) Porto, 2019 Financial support This study was supported by Fundação