TRANSFORMING GROWTH-FACTOR-BETA-1 INDUCES NEURONAL AND ASTROCYTE GENES - TUBULIN ALPHA-1, GLIAL FIBRILLARY ACIDIC PROTEIN AND CLUSTERIN

被引：101

作者：

LAPING, NJ ^{[1
]}

MORGAN, TE ^{[1
]}

NICHOLS, NR ^{[1
]}

ROZOVSKY, I ^{[1
]}

YOUNGCHAN, CS ^{[1
]}

ZAROW, C ^{[1
]}

FINCH, CE ^{[1
]}

机构：

[1] UNIV SO CALIF,ANDRUS GERONTOL CTR,LOS ANGELES,CA 90089

来源：

NEUROSCIENCE | 1994年 / 58卷 / 03期

关键词：

D O I：

10.1016/0306-4522(94)90081-7

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Transforming growth factor-beta 1 was studied as a possible regulator of messenger RNAs in astrocytes and neurons that increase after hippocampal deafferentation by perforant path transection: tubulin alpha 1, clusterin and glial fibrillary acidic protein messenger RNA. Because transforming growth factor-beta 1 messenger RNA is increased after this lesion, we examined which messenger RNA lesion responses could be induced by transforming growth factor-beta 1 alone. Porcine transforming growth factor-beta 1 infused into the lateral ventricle elevated the messenger RNAs for tubulin alpha 1, clusterin and glial fibrillary acidic protein 24 h after infusion in the ipsilateral hippocampus. As assayed by nuclear run-on, the transcription of glial fibrillary acidic protein RNA was increased in the ipsilateral hippocampus after perforant path transection and in primary rat astrocyte cultures by transforming growth factor-beta 1. In contrast, transforming growth factor-beta 1 did not change apolipoprotein-E messenger RNA or transcription, or growth associated protein-43 messenger RNA levels. We conclude that transforming growth factor-beta 1 increases subsets of neuronal and astrocyte messenger RNAs coding for cytoskeletal proteins that are also elevated in response to experimental lesions and Alzheimer's disease. This suggests that transforming growth factor-beta 1 might be a local organizing factor of neuronal and astrocyte responses to brain injury.

引用

页码：563 / 572

页数：10

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