Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain

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Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain. / Gregersen, R; Christensen, Thomas; Lehrmann, E; Diemer, Nils Henrik; Finsen, B.

In: Experimental Brain Research, Vol. 138, No. 3, 06.2001, p. 384-392.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Gregersen, R, Christensen, T, Lehrmann, E, Diemer, NH & Finsen, B 2001, 'Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain', Experimental Brain Research, vol. 138, no. 3, pp. 384-392.

APA

Gregersen, R., Christensen, T., Lehrmann, E., Diemer, N. H., & Finsen, B. (2001). Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain. Experimental Brain Research, 138(3), 384-392.

Vancouver

Gregersen R, Christensen T, Lehrmann E, Diemer NH, Finsen B. Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain. Experimental Brain Research. 2001 Jun;138(3):384-392.

Author

Gregersen, R ; Christensen, Thomas ; Lehrmann, E ; Diemer, Nils Henrik ; Finsen, B. / Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain. In: Experimental Brain Research. 2001 ; Vol. 138, No. 3. pp. 384-392.

Bibtex

@article{adc7387074c711dbbee902004c4f4f50,
title = "Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain",
abstract = "Although oligodendrocytes are vulnerable to focal cerebral ischemia, remyelination of denuded or regenerating axons in the peri-infarct area has been observed in the central nervous system. We studied the expression of myelin basic protein (MBP), a major component of central nervous system myelin, in peri-infarct areas in adult rat brain after transient middle cerebral artery occlusion (MCAO) and correlated it to the expression of the growth-associated protein-43 (GAP-43), a marker for axonal regeneration and sprouting, using non-radioactive in situ hybridization techniques. Within the infarct, MBP messenger RNA (mRNA) had disappeared by 24 h, whereas myelin protein, identified by MBP and myelin oligodendrocyte glycoprotein (MOG) immunohistochemistry, appeared structurally intact until day 3. Peri-infarct oligodendrocytes increased their expression of MBP mRNA from 24 h to maximal levels at day 7, corresponding to the appearance of process-bearing MBP and occasional MOG-immunoreactive oligodendrocytes in parallel sections. Quantitative analysis revealed significant increases in the density of oligodendrocytes (up to 7.6-fold) and in the level of MBP mRNA expressed by individual cells. Parallel sections showed that increased expression of GAP-43 mRNA in neurons was concomitant to MBP mRNA upregulation in oligodendrocytes. While the mechanisms regulating oligodendrocyte survival and myelination signals are not clear at this point, axonal sprouting could putatively serve as a stimulus for the upregulation of oligodendrocyte cell numbers, differentiation state, and/or active myelination in the peri-infarct areas.",
keywords = "Animals, Brain, Brain Ischemia, Cerebral Infarction, GAP-43 Protein, Gene Expression Regulation, Immunohistochemistry, In Situ Hybridization, Male, Myelin Basic Protein, Myelin Sheath, Nerve Degeneration, RNA, Messenger, Rats, Rats, Inbred SHR, Transcription, Genetic, Up-Regulation",
author = "R Gregersen and Thomas Christensen and E Lehrmann and Diemer, {Nils Henrik} and B Finsen",
year = "2001",
month = jun,
language = "English",
volume = "138",
pages = "384--392",
journal = "Experimental Brain Research",
issn = "0014-4819",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Focal cerebral ischemia induces increased myelin basic protein and growth-associated protein-43 gene transcription in peri-infarct areas in the rat brain

AU - Gregersen, R

AU - Christensen, Thomas

AU - Lehrmann, E

AU - Diemer, Nils Henrik

AU - Finsen, B

PY - 2001/6

Y1 - 2001/6

N2 - Although oligodendrocytes are vulnerable to focal cerebral ischemia, remyelination of denuded or regenerating axons in the peri-infarct area has been observed in the central nervous system. We studied the expression of myelin basic protein (MBP), a major component of central nervous system myelin, in peri-infarct areas in adult rat brain after transient middle cerebral artery occlusion (MCAO) and correlated it to the expression of the growth-associated protein-43 (GAP-43), a marker for axonal regeneration and sprouting, using non-radioactive in situ hybridization techniques. Within the infarct, MBP messenger RNA (mRNA) had disappeared by 24 h, whereas myelin protein, identified by MBP and myelin oligodendrocyte glycoprotein (MOG) immunohistochemistry, appeared structurally intact until day 3. Peri-infarct oligodendrocytes increased their expression of MBP mRNA from 24 h to maximal levels at day 7, corresponding to the appearance of process-bearing MBP and occasional MOG-immunoreactive oligodendrocytes in parallel sections. Quantitative analysis revealed significant increases in the density of oligodendrocytes (up to 7.6-fold) and in the level of MBP mRNA expressed by individual cells. Parallel sections showed that increased expression of GAP-43 mRNA in neurons was concomitant to MBP mRNA upregulation in oligodendrocytes. While the mechanisms regulating oligodendrocyte survival and myelination signals are not clear at this point, axonal sprouting could putatively serve as a stimulus for the upregulation of oligodendrocyte cell numbers, differentiation state, and/or active myelination in the peri-infarct areas.

AB - Although oligodendrocytes are vulnerable to focal cerebral ischemia, remyelination of denuded or regenerating axons in the peri-infarct area has been observed in the central nervous system. We studied the expression of myelin basic protein (MBP), a major component of central nervous system myelin, in peri-infarct areas in adult rat brain after transient middle cerebral artery occlusion (MCAO) and correlated it to the expression of the growth-associated protein-43 (GAP-43), a marker for axonal regeneration and sprouting, using non-radioactive in situ hybridization techniques. Within the infarct, MBP messenger RNA (mRNA) had disappeared by 24 h, whereas myelin protein, identified by MBP and myelin oligodendrocyte glycoprotein (MOG) immunohistochemistry, appeared structurally intact until day 3. Peri-infarct oligodendrocytes increased their expression of MBP mRNA from 24 h to maximal levels at day 7, corresponding to the appearance of process-bearing MBP and occasional MOG-immunoreactive oligodendrocytes in parallel sections. Quantitative analysis revealed significant increases in the density of oligodendrocytes (up to 7.6-fold) and in the level of MBP mRNA expressed by individual cells. Parallel sections showed that increased expression of GAP-43 mRNA in neurons was concomitant to MBP mRNA upregulation in oligodendrocytes. While the mechanisms regulating oligodendrocyte survival and myelination signals are not clear at this point, axonal sprouting could putatively serve as a stimulus for the upregulation of oligodendrocyte cell numbers, differentiation state, and/or active myelination in the peri-infarct areas.

KW - Animals

KW - Brain

KW - Brain Ischemia

KW - Cerebral Infarction

KW - GAP-43 Protein

KW - Gene Expression Regulation

KW - Immunohistochemistry

KW - In Situ Hybridization

KW - Male

KW - Myelin Basic Protein

KW - Myelin Sheath

KW - Nerve Degeneration

KW - RNA, Messenger

KW - Rats

KW - Rats, Inbred SHR

KW - Transcription, Genetic

KW - Up-Regulation

M3 - Journal article

C2 - 11460777

VL - 138

SP - 384

EP - 392

JO - Experimental Brain Research

JF - Experimental Brain Research

SN - 0014-4819

IS - 3

ER -

ID: 171754