Literature DB >> 1723856

Differential localization and possible functions of aFGF and bFGF in the central and peripheral nervous systems.

F Eckenstein1, W R Woodward, R Nishi.   

Abstract

We investigated the relative distribution of acidic and basic FGF (aFGF and bFGF) in the nervous system of the rat, using a combination of biological, biochemical, immunochemical, and immunohistochemical methods that can differentiate unambiguously between aFGF and bFGF. We found that different regions of the nervous system contained varying levels of aFGF and bFGF. In the central nervous system, bFGF was present nearly exclusively in astrocytes. Most neurons did not contain detectable amounts of bFGF immunoreactivity, with the notable exception of pyramidal cells in hippocampal area CA2. Interestingly, bFGF immunoreactivity was localized to the nucleus of both CA2 neurons and astrocytes. Astrocytes in vitro were also found to express bFGF, whereas cortical neurons in culture did not contain detectable amounts of bFGF. Transection of the optic nerve led to an approximately twofold increase of bFGF in the distal stump, which is consistent with the observation that bFGF is expressed by astrocytes. Transection of rat and chicken sciatic nerve resulted in a rapid and complete disappearance of aFGF from the distal nerve stump, suggesting that aFGF is present in axons projecting through the sciatic nerve. We observed, in agreement with this notion, that cultured sensory neurons contain reasonably high levels of FGF-like bioactivity. Similar levels of activity were found in developing sciatic nerve, suggesting that neuronal aFGF might be involved in regulating the development of the peripheral nervous system.

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Year:  1991        PMID: 1723856     DOI: 10.1111/j.1749-6632.1991.tb49045.x

Source DB:  PubMed          Journal:  Ann N Y Acad Sci        ISSN: 0077-8923            Impact factor:   5.691


  5 in total

1.  In Alzheimer's disease the Golgi apparatus of a population of neurons without neurofibrillary tangles is fragmented and atrophic.

Authors:  A Stieber; Z Mourelatos; N K Gonatas
Journal:  Am J Pathol       Date:  1996-02       Impact factor: 4.307

2.  FGF1 protects neuroblastoma SH-SY5Y cells from p53-dependent apoptosis through an intracrine pathway regulated by FGF1 phosphorylation.

Authors:  Caroline Pirou; Fatemeh Montazer-Torbati; Nadège Jah; Elisabeth Delmas; Christelle Lasbleiz; Bernard Mignotte; Flore Renaud
Journal:  Cell Death Dis       Date:  2017-08-31       Impact factor: 8.469

3.  Novel molecular pathways elicited by mutant FGFR2 may account for brain abnormalities in Apert syndrome.

Authors:  Erika Yeh; Roberto D Fanganiello; Daniele Y Sunaga; Xueyan Zhou; Gregory Holmes; Katia M Rocha; Nivaldo Alonso; Hamilton Matushita; Yingli Wang; Ethylin W Jabs; Maria Rita Passos-Bueno
Journal:  PLoS One       Date:  2013-04-04       Impact factor: 3.240

4.  Tricyclic antidepressant amitriptyline indirectly increases the proliferation of adult dentate gyrus-derived neural precursors: an involvement of astrocytes.

Authors:  Shuken Boku; Kazue Hisaoka-Nakashima; Shin Nakagawa; Akiko Kato; Naoto Kajitani; Takeshi Inoue; Ichiro Kusumi; Minoru Takebayashi
Journal:  PLoS One       Date:  2013-11-18       Impact factor: 3.240

5.  FGF1 C-terminal domain and phosphorylation regulate intracrine FGF1 signaling for its neurotrophic and anti-apoptotic activities.

Authors:  E Delmas; N Jah; C Pirou; S Bouleau; N Le Floch; J-L Vayssière; B Mignotte; F Renaud
Journal:  Cell Death Dis       Date:  2016-02-04       Impact factor: 8.469

  5 in total

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