title: Transforming growth factor-beta 1 induces neuronal and astrocyte genes: tubulin alpha 1, glial fibrillary acidic protein and clusterin.
abstract: 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.
authors.affiliation: Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191.
authors.forename: N J
authors.initials: NJ
authors.lastname: Laping
authors.forename: T E
authors.initials: TE
authors.lastname: Morgan
authors.forename: N R
authors.initials: NR
authors.lastname: Nichols
authors.forename: I
authors.initials: I
authors.lastname: Rozovsky
authors.forename: C S
authors.initials: CS
authors.lastname: Young-Chan
authors.forename: C
authors.initials: C
authors.lastname: Zarow
authors.forename: C E
authors.initials: CE
authors.lastname: Finch
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000096:biosynthesis / Q000235:genetics; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001483:Base Sequence; D015152:Blotting, Northern; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D002478:Cells, Cultured; D051152:Clusterin; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis* / Q000235:genetics; D006023:Glycoproteins / Q000096:biosynthesis* / Q000235:genetics; D017403:In Situ Hybridization; D008297:Male; D018832:Molecular Chaperones; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics; D009473:Neuronal Plasticity / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011916:Rats, Inbred F344; D013569:Synapses / Q000187:drug effects; D014158:Transcription, Genetic / Q000187:drug effects; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D014404:Tubulin / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D001057:Apolipoproteins E; D051152:Clusterin; D005904:Glial Fibrillary Acidic Protein; D006023:Glycoproteins; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D014404:Tubulin