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Titolo:
Antisense prevention of neuronal damages following head injury in mice
Autore:
Shohami, E; Kaufer, D; Chen, Y; Seidman, S; Cohen, O; Ginzberg, D; Melamed-Book, N; Yirmiya, R; Soreq, H;
Indirizzi:
Hebrew Univ Jerusalem, Fac Social Sci, Inst Life Sci, Dept Biol Chem, IL-91904 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91904 -91904 Jerusalem, Israel Hebrew Univ Jerusalem, Fac Social Sci, Sch Pharm, Dept Pharmacol, IL-91904Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91904 L-91904Jerusalem, Israel Hebrew Univ Jerusalem, Fac Social Sci, Dept Psychol, IL-91904 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91904 -91904 Jerusalem, Israel
Titolo Testata:
JOURNAL OF MOLECULAR MEDICINE-JMM
fascicolo: 4, volume: 78, anno: 2000,
pagine: 228 - 236
SICI:
0946-2716(2000)78:4<228:APONDF>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACETYLCHOLINESTERASE-TRANSGENIC MICE; TRAUMATIC BRAIN INJURY; GENE-EXPRESSION; STRESS; HIPPOCAMPUS; DETERIORATION; STRATEGIES; PATHOLOGY; PROTEIN; CORTEX;
Keywords:
antisense; oligonucleotides; head injury; acetylcholinesterase; emergency medicine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Soreq, H Hebrew Univ Jerusalem, Fac Social Sci, Inst Life Sci, Dept Biol Chem, IL-91904 Jerusalem, Israel Hebrew Univ Jerusalem Jerusalem Israel IL-91904 rusalem, Israel
Citazione:
E. Shohami et al., "Antisense prevention of neuronal damages following head injury in mice", J MOL MED-J, 78(4), 2000, pp. 228-236

Abstract

Closed head injury (CHI) is an important cause of death among young adultsand a prominent risk factor for nonfamilial Alzheimer's disease. Emergencyintervention following CHI should therefore strive to improve survival, promote recovery, and prevent delayed neuropathologies. We employed high-resolution nonradioactive in situ hybridization to determine whether a single intracerebroventricular injection of 500 ng 2'-O-methyl RNA-capped antisenseoligonucleotide (AS-ODN) against acetylcholinesterase (AChE) mRNA blocks overexpression of the stress-related readthrough AChE (AChE-R) mRNA splicingvariant in head-injured mice. Silver-based Golgi staining revealed pronounced dendrite outgrowth in somatosensory cortex of traumatized mice 14 days postinjury that was associated with sites of AChE-R mRNA overexpression andsuppressed by anti-AChE AS-ODNs. Furthermore, antisense treatment reduced the number of dead CA3 hippocampal neurons in injured mice, and facilitatedneurological recovery as determined by performance in tests of neuromotor coordination. In trauma-sensitive transgenic mice overproducing AChE, antisense treatment reduced mortality from 50% to 20%, similar to that displayedby head-injured control mice. These findings demonstrate the potential of antisense therapeutics in treating acute injury, and suggest antisense prevention of AChE-R overproduction to mitigate the detrimental consequences ofvarious traumatic brain insults.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 17:26:06