The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish.

Y-M Yu; M Cristofanilli; A Valiveti; L Ma; M Yoo; Fabio Morellini; Melitta Schachner

The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish.

Standard

The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish. / Yu, Y-M; Cristofanilli, M; Valiveti, A; Ma, L; Yoo, M; Morellini, Fabio; Schachner, Melitta.

in: NEUROSCIENCE, Jahrgang 183, 2011, S. 238-250.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Yu, Y-M, Cristofanilli, M, Valiveti, A, Ma, L, Yoo, M, Morellini, F & Schachner, M 2011, 'The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish.', NEUROSCIENCE, Jg. 183, S. 238-250. <http://www.ncbi.nlm.nih.gov/pubmed/21443931?dopt=Citation>

APA

Yu, Y-M., Cristofanilli, M., Valiveti, A., Ma, L., Yoo, M., Morellini, F., & Schachner, M. (2011). The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish. NEUROSCIENCE, 183, 238-250. http://www.ncbi.nlm.nih.gov/pubmed/21443931?dopt=Citation

Vancouver

Yu Y-M, Cristofanilli M, Valiveti A, Ma L, Yoo M, Morellini F et al. The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish. NEUROSCIENCE. 2011;183:238-250.

Bibtex

@article{a062b6007f654686b446b4e6f7628fd4,

title = "The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish.",

abstract = "Adult zebrafish, by virtue of exhibiting spontaneous recovery after spinal lesion, have evolved into a paradigmatic vertebrate model system to identify novel genes vital for successful regeneration after spinal cord injury. Due to a remarkable level of conservation between zebrafish and human genomes, such genes, once identified, could point to possibilities for addressing the multiple issues on how to deal with functional recovery after spinal cord injury in humans. In the current study, the extracellular matrix glycoprotein tenascin-C was studied in the zebrafish spinal cord injury model to assess the often disparate functions of this multidomain molecule under in vivo conditions. This in vivo study was deemed necessary since in vitro studies had shown discrepant functional effects on neurite outgrowth: tenascin-C inhibits neurite outgrowth when presented as a molecular barrier adjacent to a conducive substrate, but enhances neurite outgrowth when presented as a uniform substrate. Thus, our current study addresses the question as to which of these features prevails in vivo: whether tenascin-C reduces or enhances axonal regrowth after injury in a well accepted vertebrate model of spinal cord injury. We show upregulation of tenascin-C expression in regenerating neurons of the nucleus of median longitudinal fascicle (NMLF) in the brainstem and spinal motoneurons. Inhibition of tenascin-C expression by antisense oligonucleotide (morpholino) resulted in impaired locomotor recovery, reduced regrowth of axons from brainstem neurons and reduced synapse formation by the regrowing brainstem axons on spinal motoneurons, all vital indicators of regeneration. Our results thus point to an advantageous role of tenascin-C in promoting spinal cord regeneration, by promoting axonal regrowth and synapse formation in the spinal cord caudal to the lesion site after injury.",

keywords = "Animals, Humans, Disease Models, Animal, Analysis of Variance, Cell Count, Motor Activity/*drug effects, RNA, Messenger/metabolism, Neural Pathways/pathology, Choline O-Acetyltransferase/metabolism, Brain Stem/pathology, Indoles/diagnostic use, Lysine/analogs & derivatives/metabolism, Membrane Glycoproteins/metabolism, Motor Neurons/metabolism, Nerve Regeneration/*drug effects, Oligodeoxyribonucleotides, Antisense/therapeutic use, Recovery of Function/drug effects/physiology, Spinal Cord Injuries/drug therapy/*metabolism/pathology/*physiopathology, Synapses/pathology, Tenascin/genetics/*metabolism, Transcription Factors/metabolism, Up-Regulation/drug effects/physiology, Zebrafish, Zebrafish Proteins/metabolism, Animals, Humans, Disease Models, Animal, Analysis of Variance, Cell Count, Motor Activity/*drug effects, RNA, Messenger/metabolism, Neural Pathways/pathology, Choline O-Acetyltransferase/metabolism, Brain Stem/pathology, Indoles/diagnostic use, Lysine/analogs & derivatives/metabolism, Membrane Glycoproteins/metabolism, Motor Neurons/metabolism, Nerve Regeneration/*drug effects, Oligodeoxyribonucleotides, Antisense/therapeutic use, Recovery of Function/drug effects/physiology, Spinal Cord Injuries/drug therapy/*metabolism/pathology/*physiopathology, Synapses/pathology, Tenascin/genetics/*metabolism, Transcription Factors/metabolism, Up-Regulation/drug effects/physiology, Zebrafish, Zebrafish Proteins/metabolism",

author = "Y-M Yu and M Cristofanilli and A Valiveti and L Ma and M Yoo and Fabio Morellini and Melitta Schachner",

year = "2011",

language = "English",

volume = "183",

pages = "238--250",

journal = "NEUROSCIENCE",

issn = "0306-4522",

publisher = "Elsevier Limited",

}

RIS

TY - JOUR

T1 - The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish.

AU - Yu, Y-M

AU - Cristofanilli, M

AU - Valiveti, A

AU - Ma, L

AU - Yoo, M

AU - Morellini, Fabio

AU - Schachner, Melitta

PY - 2011

Y1 - 2011

N2 - Adult zebrafish, by virtue of exhibiting spontaneous recovery after spinal lesion, have evolved into a paradigmatic vertebrate model system to identify novel genes vital for successful regeneration after spinal cord injury. Due to a remarkable level of conservation between zebrafish and human genomes, such genes, once identified, could point to possibilities for addressing the multiple issues on how to deal with functional recovery after spinal cord injury in humans. In the current study, the extracellular matrix glycoprotein tenascin-C was studied in the zebrafish spinal cord injury model to assess the often disparate functions of this multidomain molecule under in vivo conditions. This in vivo study was deemed necessary since in vitro studies had shown discrepant functional effects on neurite outgrowth: tenascin-C inhibits neurite outgrowth when presented as a molecular barrier adjacent to a conducive substrate, but enhances neurite outgrowth when presented as a uniform substrate. Thus, our current study addresses the question as to which of these features prevails in vivo: whether tenascin-C reduces or enhances axonal regrowth after injury in a well accepted vertebrate model of spinal cord injury. We show upregulation of tenascin-C expression in regenerating neurons of the nucleus of median longitudinal fascicle (NMLF) in the brainstem and spinal motoneurons. Inhibition of tenascin-C expression by antisense oligonucleotide (morpholino) resulted in impaired locomotor recovery, reduced regrowth of axons from brainstem neurons and reduced synapse formation by the regrowing brainstem axons on spinal motoneurons, all vital indicators of regeneration. Our results thus point to an advantageous role of tenascin-C in promoting spinal cord regeneration, by promoting axonal regrowth and synapse formation in the spinal cord caudal to the lesion site after injury.

AB - Adult zebrafish, by virtue of exhibiting spontaneous recovery after spinal lesion, have evolved into a paradigmatic vertebrate model system to identify novel genes vital for successful regeneration after spinal cord injury. Due to a remarkable level of conservation between zebrafish and human genomes, such genes, once identified, could point to possibilities for addressing the multiple issues on how to deal with functional recovery after spinal cord injury in humans. In the current study, the extracellular matrix glycoprotein tenascin-C was studied in the zebrafish spinal cord injury model to assess the often disparate functions of this multidomain molecule under in vivo conditions. This in vivo study was deemed necessary since in vitro studies had shown discrepant functional effects on neurite outgrowth: tenascin-C inhibits neurite outgrowth when presented as a molecular barrier adjacent to a conducive substrate, but enhances neurite outgrowth when presented as a uniform substrate. Thus, our current study addresses the question as to which of these features prevails in vivo: whether tenascin-C reduces or enhances axonal regrowth after injury in a well accepted vertebrate model of spinal cord injury. We show upregulation of tenascin-C expression in regenerating neurons of the nucleus of median longitudinal fascicle (NMLF) in the brainstem and spinal motoneurons. Inhibition of tenascin-C expression by antisense oligonucleotide (morpholino) resulted in impaired locomotor recovery, reduced regrowth of axons from brainstem neurons and reduced synapse formation by the regrowing brainstem axons on spinal motoneurons, all vital indicators of regeneration. Our results thus point to an advantageous role of tenascin-C in promoting spinal cord regeneration, by promoting axonal regrowth and synapse formation in the spinal cord caudal to the lesion site after injury.

KW - Animals

KW - Humans

KW - Disease Models, Animal

KW - Analysis of Variance

KW - Cell Count

KW - Motor Activity/drug effects

KW - RNA, Messenger/metabolism

KW - Neural Pathways/pathology

KW - Choline O-Acetyltransferase/metabolism

KW - Brain Stem/pathology

KW - Indoles/diagnostic use

KW - Lysine/analogs & derivatives/metabolism

KW - Membrane Glycoproteins/metabolism

KW - Motor Neurons/metabolism

KW - Nerve Regeneration/drug effects

KW - Oligodeoxyribonucleotides, Antisense/therapeutic use

KW - Recovery of Function/drug effects/physiology

KW - Spinal Cord Injuries/drug therapy/metabolism/pathology/physiopathology

KW - Synapses/pathology

KW - Tenascin/genetics/metabolism

KW - Transcription Factors/metabolism

KW - Up-Regulation/drug effects/physiology

KW - Zebrafish

KW - Zebrafish Proteins/metabolism