Abstract：
:Insulin-like growth factors, IGF-I and IGF-II, are potent regulators of oligodendrocyte development. Most of the IGF present in vivo is bound to members of a family of six high-affinity IGF-binding proteins (IGFBPs), which can either potentiate or inhibit IGF action, depending on other conditions. Additionally, serum contains a structurally unrelated protein, acid-labile sub-unit (ALS), which forms a ternary complex with IGF and IGFBP3. In this study, we used reverse-transcriptase polymerase chain reaction (RT-PCR) to examine the expression of mRNAs for IGFBP 1-6 and ALS in purified populations of oligodendroglial cells and astrocytes. We found that astrocytes express all six IGFBPs. A2B5+/O4- oligodendrocyte precursors, O4+/O1- intermediate precursors, and O1+ oligodendrocytes express IGFBP3, 5, and 6, while IGFBP4 is expressed in oligodendrocyte precursors but not at more mature stages. We were unable to detect ALS mRNA in whole brain or in cultured oligodendroglial cells. The presence of differentially expressed IGFBPs in developing oligodendrocytes and astrocytes could significantly affect the biological activity of IGF-I and IGF-II in the central nervous system and the IGF-responsiveness of the IGFBP-expressing cells.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Mewar R,McMorris FAdoi
10.1002/(SICI)1097-4547(19971201)50:5<721::AID-JNRsubject
Has Abstractpub_date
1997-12-01 00:00:00pages
721-8issue
5eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19971201)50:5<721::AID-JNRjournal_volume
50pub_type
杂志文章abstract：:Adrenal chromaffin cell (ACC) transplants, alone or combined with levodopa treatment, were used in attempted therapy for Parkinson's disease (PD). In a previous study, we demonstrated that levodopa caused chromaffin cell death either by necrosis or by apoptosis in cell culture. Here we report the beneficial effect of ...
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doi：10.1002/1097-4547(20000915)61:6<636::AID-JNR7>3.0.
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journal_title：Journal of neuroscience research
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doi：
更新日期：1997-08-15 00:00:00
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更新日期：2004-04-01 00:00:00
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doi：10.1002/jnr.490420402
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pub_type： 杂志文章
doi：10.1002/jnr.490320313
更新日期：1992-07-01 00:00:00
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更新日期：1992-02-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/(SICI)1097-4547(19971201)50:5<829::AID-JNR
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.490270421
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journal_title：Journal of neuroscience research
pub_type： 杂志文章,评审
doi：10.1002/jnr.490410202
更新日期：1995-06-01 00:00:00
abstract：:Mice heterozygously deficient in the major myelin component P0 are an established model of an inherited neuropathy and show signs of myelin degeneration in motor nerves. Unlike the case in patients, the sensory nerves are only mildly affected in the mouse mutants and do not show features indicative of myelin degenerat...
journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.10115
更新日期：2002-01-15 00:00:00
abstract：:GM1, GD1a, and GT1b inhibit both PDGF-stimulated and serum-stimulated DNA synthesis in Swiss 3T3 cells and the human glioma cell line U-1242 MG in a dose-dependent manner. The ganglioside inhibitory effect is counteracted in a dose-responsive fashion by serum such that ganglioside-induced inhibition is essentially abo...
journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.490410408
更新日期：1995-07-01 00:00:00
