Literature DB >> 17569064

Gene expression analysis of frontotemporal lobar degeneration of the motor neuron disease type with ubiquitinated inclusions.

Manjari Mishra1, Tatjana Paunesku, Gayle E Woloschak, Teepu Siddique, Lihua Julie Zhu, Simon Lin, Kristin Greco, Eileen H Bigio.   

Abstract

Neurodegenerative disorders share a process of aggregation of insoluble protein. Frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U) is characterized by the presence of ubiquitin and TDP-43 positive aggregates which are likely related to specific gene expression profiles. We carried out gene expression microarray analysis on post-mortem brain tissue from FTLD-U, FTLD-MND, and controls. Using total RNA from carefully dissected frontal cortical layer II, we obtained gene expression profiles showing that FTLD-U and controls differ in over 100 networks, including those involved in synapse formation, the ubiquitin-proteasome system, endosomal sorting, and apoptosis. We performed qRT-PCR validation for three genes, representative of three different networks. Dynein axonemal light intermediate chain 1 (DNALI1) (microtubule/cytoskeleton network associated) expression was 3-fold higher and myeloid differentiation primary response gene 88 (MYD88) (signal transduction network) was 3.3 times higher in FTLD-U than FTLD-MND and controls; annexin A2 (ANXA2) (endosomal sorting) expression was 11.3-fold higher in FTLD-U than FTLD-MND and 2.3-fold higher than controls. The identification of progranulin (PGRN) gene mutations and TDP-43 as the major protein component of the ubiquitinated inclusions, are two recent landmark discoveries in the field of FTLD-U. We found 1.5-fold increase in TDP-43 in both FTLD-MND and FTLD-U while progranulin showed no gene expression differences between controls and FTLD-MND. However, one of the FTLD-U cases tested by Affymetrix microarray showed "absence call" of this transcript, suggesting absent or decreased gene expression. Our findings point to specific gene-linked-pathways which may be influenced by neurodegenerative disease process and may be targeted for further exploration.

Entities:  

Mesh:

Substances:

Year:  2007        PMID: 17569064     DOI: 10.1007/s00401-007-0240-7

Source DB:  PubMed          Journal:  Acta Neuropathol        ISSN: 0001-6322            Impact factor:   17.088


  41 in total

1.  Identification of active loci of a human endogenous retrovirus in neurons of patients with amyotrophic lateral sclerosis.

Authors:  Renée Douville; Jiankai Liu; Jeffrey Rothstein; Avindra Nath
Journal:  Ann Neurol       Date:  2011-01       Impact factor: 10.422

Review 2.  Update on recent molecular and genetic advances in frontotemporal lobar degeneration.

Authors:  Eileen H Bigio
Journal:  J Neuropathol Exp Neurol       Date:  2008-07       Impact factor: 3.685

Review 3.  TDP-43 autoregulation: implications for disease.

Authors:  Mauricio Budini; Emanuele Buratti
Journal:  J Mol Neurosci       Date:  2011-06-18       Impact factor: 3.444

4.  VCP mutations causing frontotemporal lobar degeneration disrupt localization of TDP-43 and induce cell death.

Authors:  Michael A Gitcho; Jeffrey Strider; Deborah Carter; Lisa Taylor-Reinwald; Mark S Forman; Alison M Goate; Nigel J Cairns
Journal:  J Biol Chem       Date:  2009-02-23       Impact factor: 5.157

5.  cNEUPRO: Novel Biomarkers for Neurodegenerative Diseases.

Authors:  Philipp Spitzer; Hans Wolfgang Klafki; Kaj Blennow; Luc Buée; Hermann Esselmann; Sanna-Kaisa Herruka; Connie Jimenez; Peter Klivenyi; Piotr Lewczuk; Juan Manuel Maler; Katrin Markus; Helmut E Meyer; Chris Morris; Thorsten Müller; Markus Otto; Lucilla Parnetti; Hilkka Soininen; Susanna Schraen; Charlotte Teunissen; Laszlo Vecsei; Henrik Zetterberg; Jens Wiltfang
Journal:  Int J Alzheimers Dis       Date:  2010-09-19

Review 6.  Annexin A2 system in human biology: cell surface and beyond.

Authors:  Min Luo; Katherine A Hajjar
Journal:  Semin Thromb Hemost       Date:  2013-03-12       Impact factor: 4.180

Review 7.  Amyotrophic lateral sclerosis, frontotemporal dementia and beyond: the TDP-43 diseases.

Authors:  Felix Geser; Maria Martinez-Lage; Linda K Kwong; Virginia M-Y Lee; John Q Trojanowski
Journal:  J Neurol       Date:  2009-03-07       Impact factor: 4.849

8.  The JNK/c-Jun signaling axis contributes to the TDP-43-induced cell death.

Authors:  Hiroaki Suzuki; Masaaki Matsuoka
Journal:  Mol Cell Biochem       Date:  2012-09-24       Impact factor: 3.396

9.  Mitochondrial dysfunction and decrease in body weight of a transgenic knock-in mouse model for TDP-43.

Authors:  Carola Stribl; Aladin Samara; Dietrich Trümbach; Regina Peis; Manuela Neumann; Helmut Fuchs; Valerie Gailus-Durner; Martin Hrabě de Angelis; Birgit Rathkolb; Eckhard Wolf; Johannes Beckers; Marion Horsch; Frauke Neff; Elisabeth Kremmer; Sebastian Koob; Andreas S Reichert; Wolfgang Hans; Jan Rozman; Martin Klingenspor; Michaela Aichler; Axel Karl Walch; Lore Becker; Thomas Klopstock; Lisa Glasl; Sabine M Hölter; Wolfgang Wurst; Thomas Floss
Journal:  J Biol Chem       Date:  2014-02-10       Impact factor: 5.157

10.  Sporadic ALS has compartment-specific aberrant exon splicing and altered cell-matrix adhesion biology.

Authors:  Stuart J Rabin; Jae Mun Hugo Kim; Michael Baughn; Ryan T Libby; Young Joo Kim; Yuxin Fan; Randell T Libby; Albert La Spada; Brad Stone; John Ravits
Journal:  Hum Mol Genet       Date:  2009-10-28       Impact factor: 6.150

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.