VEGF is a modifier of amyotrophic lateral sclerosis in mice and humans and protects motoneurons against ischemic death
Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa δ/δ mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium an...
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| Vydáno v: | Nature genetics Ročník 34; číslo 4; s. 383 - 394 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
New York
Nature Publishing Group US
01.08.2003
Nature Publishing Group |
| Témata: | |
| ISSN: | 1061-4036, 1546-1718 |
| On-line přístup: | Získat plný text |
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| Abstract | Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of
Vegfa
causes ALS-like motoneuron degeneration in
Vegfa
δ/δ
mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes −2,578A/−1,154A/−634G or −2,578A/−1,154G/−634G in the
VEGF
promoter/leader sequence had a 1.8 times greater risk of ALS (
P
= 0.00004). These 'at-risk' haplotypes lowered circulating VEGF levels
in vivo
and reduced
VEGF
gene transcription, IRES-mediated
VEGF
expression and translation of a novel large-VEGF isoform (L-VEGF)
in vivo
. Moreover,
SOD1
G93A
mice crossbred with
Vegfa
δ/δ
mice died earlier due to more severe motoneuron degeneration. Vegfa
δ/δ
mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that
VEGF
is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice. |
|---|---|
| AbstractList | Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa(delta/delta) mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes -2,578A/-1,154A/-634G or -2,578A/-1,154G/-634G in the VEGF promoter/leader sequence had a 1.8 times greater risk of ALS (P = 0.00004). These 'at-risk' haplotypes lowered circulating VEGF levels in vivo and reduced VEGF gene transcription, IRES-mediated VEGF expression and translation of a novel large-VEGF isoform (L-VEGF) in vivo. Moreover, SOD1(G93A) mice crossbred with Vegfa(delta/delta) mice died earlier due to more severe motoneuron degeneration. Vegfa(delta/delta) mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that VEGF is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice.Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa(delta/delta) mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes -2,578A/-1,154A/-634G or -2,578A/-1,154G/-634G in the VEGF promoter/leader sequence had a 1.8 times greater risk of ALS (P = 0.00004). These 'at-risk' haplotypes lowered circulating VEGF levels in vivo and reduced VEGF gene transcription, IRES-mediated VEGF expression and translation of a novel large-VEGF isoform (L-VEGF) in vivo. Moreover, SOD1(G93A) mice crossbred with Vegfa(delta/delta) mice died earlier due to more severe motoneuron degeneration. Vegfa(delta/delta) mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that VEGF is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice. Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa(delta/delta) mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes -2,578A/-1,154A/-634G or -2,578A/-1,154G/-634G in the VEGF promoter/leader sequence had a 1.8 times greater risk of ALS (P = 0.00004). These 'at-risk' haplotypes lowered circulating VEGF levels in vivo and reduced VEGF gene transcription, IRES-mediated VEGF expression and translation of a novel large-VEGF isoform (L-VEGF) in vivo. Moreover, SOD1(G93A) mice crossbred with Vegfa(delta/delta) mice died earlier due to more severe motoneuron degeneration. Vegfa(delta/delta) mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that VEGF is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice. Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa δ/δ mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes −2,578A/−1,154A/−634G or −2,578A/−1,154G/−634G in the VEGF promoter/leader sequence had a 1.8 times greater risk of ALS ( P = 0.00004). These 'at-risk' haplotypes lowered circulating VEGF levels in vivo and reduced VEGF gene transcription, IRES-mediated VEGF expression and translation of a novel large-VEGF isoform (L-VEGF) in vivo . Moreover, SOD1 G93A mice crossbred with Vegfa δ/δ mice died earlier due to more severe motoneuron degeneration. Vegfa δ/δ mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that VEGF is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice. Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like motoneuron degeneration in Vegfa super( delta / delta ) mice. In a meta-analysis of over 900 individuals from Sweden and over 1,000 individuals from Belgium and England, we now report that subjects homozygous with respect to the haplotypes -2,578A/-1,154A/-634G or -2,578A/-1,154G/-634G in the VEGF promoter/leader sequence had a 1.8 times greater risk of ALS (P = 0.00004). These `at-risk' haplotypes lowered circulating VEGF levels in vivo and reduced VEGF gene transcription, IRES-mediated VEGF expression and translation of a novel large-VEGF isoform (L-VEGF) in vivo. Moreover, SOD1 super(G93A) mice crossbred with Vegfa super( delta / delta ) mice died earlier due to more severe motoneuron degeneration. Vegfa super( delta / delta ) mice were unusually susceptible to persistent paralysis after spinal cord ischemia, and treatment with Vegfa protected mice against ischemic motoneuron death. These findings indicate that VEGF is a modifier of motoneuron degeneration in human ALS and unveil a therapeutic potential of Vegfa for stressed motoneurons in mice. |
| Audience | Academic |
| Author | Morrison, Karen E Wyns, Sabine Bornes, Stephanie Katayama, Shigehiro Vermeire, Severine Lang-Lazdunski, Loïc Robberecht, Wim Andersson, Jörgen Rutgeerts, Paul Al-Chalabi, Ammar Storkebaum, Erik Adolfsson, Rolf Pall, Hardev Singh Andersen, Peter M Lambrechts, Diether Beckman, Lars Prats, Hervé Carmeliet, Peter van Marion, Ingrid Collen, Désiré Hansen, Valerie Thijs, Vincent Shaw, Christopher Vlietinck, Robert Del-Favero, Jurgen Dewerchin, Mieke Leigh, Nigel Musson, Rhiannon Marklund, Stefan L Desmet, Frederik Awata, Takuya Van Broeckhoven, Christine Morimoto, Masafumi Moons, Lieve |
| Author_xml | – sequence: 1 givenname: Diether surname: Lambrechts fullname: Lambrechts, Diether organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 2 givenname: Erik surname: Storkebaum fullname: Storkebaum, Erik organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 3 givenname: Masafumi surname: Morimoto fullname: Morimoto, Masafumi organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 4 givenname: Jurgen surname: Del-Favero fullname: Del-Favero, Jurgen organization: Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp – sequence: 5 givenname: Frederik surname: Desmet fullname: Desmet, Frederik organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 6 givenname: Stefan L surname: Marklund fullname: Marklund, Stefan L organization: Department of Neurology, Umea University Hospital, and Institute of Clinical Neuroscience and Medical Genetics, Umea University – sequence: 7 givenname: Sabine surname: Wyns fullname: Wyns, Sabine organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 8 givenname: Vincent surname: Thijs fullname: Thijs, Vincent organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 9 givenname: Jörgen surname: Andersson fullname: Andersson, Jörgen organization: Department of Neurology, Umea University Hospital, and Institute of Clinical Neuroscience and Medical Genetics, Umea University – sequence: 10 givenname: Ingrid surname: van Marion fullname: van Marion, Ingrid organization: Department of Neurology, The Medical School, University of Birmingham – sequence: 11 givenname: Ammar surname: Al-Chalabi fullname: Al-Chalabi, Ammar organization: Departments of Neurology and Medical and Molecular Genetics, Guy's, King's and St. Thomas' School of Medicine and Institute of Psychiatry, King's College London – sequence: 12 givenname: Stephanie surname: Bornes fullname: Bornes, Stephanie organization: INSERM 397, Endocrinologie et Communication Cellulaire, Institut Fédératif de Recherche Louis Bugnard, CHU Rangueil – sequence: 13 givenname: Rhiannon surname: Musson fullname: Musson, Rhiannon organization: Department of Neurology, The Medical School, University of Birmingham – sequence: 14 givenname: Valerie surname: Hansen fullname: Hansen, Valerie organization: Departments of Neurology and Medical and Molecular Genetics, Guy's, King's and St. Thomas' School of Medicine and Institute of Psychiatry, King's College London – sequence: 15 givenname: Lars surname: Beckman fullname: Beckman, Lars organization: Department of Neurology, Umea University Hospital, and Institute of Clinical Neuroscience and Medical Genetics, Umea University – sequence: 16 givenname: Rolf surname: Adolfsson fullname: Adolfsson, Rolf organization: Department of Clinical Sciences, Division of Psychiatry, Umea University – sequence: 17 givenname: Hardev Singh surname: Pall fullname: Pall, Hardev Singh organization: Department of Neurology, The Medical School, University of Birmingham – sequence: 18 givenname: Hervé surname: Prats fullname: Prats, Hervé organization: INSERM 397, Endocrinologie et Communication Cellulaire, Institut Fédératif de Recherche Louis Bugnard, CHU Rangueil – sequence: 19 givenname: Severine surname: Vermeire fullname: Vermeire, Severine organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 20 givenname: Paul surname: Rutgeerts fullname: Rutgeerts, Paul organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 21 givenname: Shigehiro surname: Katayama fullname: Katayama, Shigehiro organization: 4th Department of Medicine, Saitama Medical School, Moroyama – sequence: 22 givenname: Takuya surname: Awata fullname: Awata, Takuya organization: 4th Department of Medicine, Saitama Medical School, Moroyama – sequence: 23 givenname: Nigel surname: Leigh fullname: Leigh, Nigel organization: Departments of Neurology and Medical and Molecular Genetics, Guy's, King's and St. Thomas' School of Medicine and Institute of Psychiatry, King's College London – sequence: 24 givenname: Loïc surname: Lang-Lazdunski fullname: Lang-Lazdunski, Loïc organization: Service de Chirurgie Thoracique, Hôpital Européen Georges Pompidou – sequence: 25 givenname: Mieke surname: Dewerchin fullname: Dewerchin, Mieke organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 26 givenname: Christopher surname: Shaw fullname: Shaw, Christopher organization: Departments of Neurology and Medical and Molecular Genetics, Guy's, King's and St. Thomas' School of Medicine and Institute of Psychiatry, King's College London – sequence: 27 givenname: Lieve surname: Moons fullname: Moons, Lieve organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 28 givenname: Robert surname: Vlietinck fullname: Vlietinck, Robert organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg, Department of Population Genetics, Genomics & Bioinformatics, University Maastricht – sequence: 29 givenname: Karen E surname: Morrison fullname: Morrison, Karen E organization: Department of Neurology, The Medical School, University of Birmingham – sequence: 30 givenname: Wim surname: Robberecht fullname: Robberecht, Wim organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 31 givenname: Christine surname: Van Broeckhoven fullname: Van Broeckhoven, Christine organization: Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp – sequence: 32 givenname: Désiré surname: Collen fullname: Collen, Désiré organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg – sequence: 33 givenname: Peter M surname: Andersen fullname: Andersen, Peter M organization: Department of Neurology, Umea University Hospital, and Institute of Clinical Neuroscience and Medical Genetics, Umea University – sequence: 34 givenname: Peter surname: Carmeliet fullname: Carmeliet, Peter email: peter.carmeliet@med.kuleuven.ac.be organization: Flanders Interuniversity Institute for Biotechnology and Departments of Neurology and Internal Medicine, The Center for Transgene Technology and Gene Therapy, University Hospital Gasthuisberg |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15048557$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/12847526$$D View this record in MEDLINE/PubMed |
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| Snippet | Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of
Vegfa
causes ALS-like... Amyotrophic lateral sclerosis (ALS) is an incurable degenerative disorder of motoneurons. We recently reported that reduced expression of Vegfa causes ALS-like... |
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| SubjectTerms | Aged Agriculture Alleles Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - drug therapy Amyotrophic Lateral Sclerosis - etiology Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - pathology Animal Genetics and Genomics Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Cell Death - drug effects Cerebrospinal fluid. Meninges. Spinal cord Child Child, Preschool Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Diagnosis Embryology: invertebrates and vertebrates. Teratology Endothelial Growth Factors - genetics Endothelial Growth Factors - physiology Endothelial Growth Factors - therapeutic use Female Fundamental and applied biological sciences. Psychology Gene Function Genes Genetic aspects Genetic Variation Genetics Haplotypes Human Genetics Humans Hypoxia Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - physiology Intercellular Signaling Peptides and Proteins - therapeutic use Ischemia Ischemia - pathology Lymphokines - genetics Lymphokines - physiology Lymphokines - therapeutic use Male Medical sciences Mice Mice, Knockout Mice, Transgenic Middle Aged Molecular embryology Mortality Motor neurons Motor Neurons - drug effects Motor Neurons - pathology Mutation Nerve Degeneration - genetics Nervous system (semeiology, syndromes) Neurology Paralysis - etiology Pathogenesis Physiological aspects Risk factors Spinal cord Spinal Cord Ischemia - drug therapy Spinal Cord Ischemia - pathology Sweden Vascular endothelial growth factor Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| Title | VEGF is a modifier of amyotrophic lateral sclerosis in mice and humans and protects motoneurons against ischemic death |
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