Increased basic fibroblast growth factor (bFGF) immunoreactivity at the site of focal brain wounds

Finklestein, Seth P.; Apostolides, Paul J.; Caday, Cornelio G.; Prosser, James I.; Philips, Matthew F.; Klagsbrun, Michael

doi:10.1016/0006-8993(88)90370-8

Cited by 370 publications

(130 citation statements)

References 25 publications

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“…Neurotrophic factors are produced around the locus of CNS lesions, and although earlier studies did not identify the source of these factors (NietoSampedro et al, 1982(NietoSampedro et al, , 1983Needels et al, 1986;Ernfors et al, 1989;Ishikawa et al, 1991;Lindvall et al, 1994), more recent studies have documented the upregulation of nerve growth factor (NGF) (Bakhit et al, 1991;Altar et al, 1992;Oderfeld-Nowak et al, 1992;Arendt et al, 1995), ciliary neurotrophic factor (Ip et al, 1993;Asada et al, 1995;Wen et al, 1995), basic fibroblast growth factor (Finklestein et al, 1988;Frautschy et al, 1991;GomezPinilla et al, 1995;Wen et al, 1995), and insulin-like growth factor-1 (Komoly et al, 1992) in reactive astrocytes.…”

Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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The relevance of astrogliosis remains controversial, especially with respect to the beneficial or detrimental influence of reactive astrocytes on CNS recovery. This dichotomy can be resolved if the mediators of astrogliosis are identified. We have measured the levels of transcripts encoding inflammatory cytokines in injury systems in which the presence or absence of astrogliosis could be produced selectively. A stab injury to the adult mouse brain using a piece of nitrocellulose (NC) membrane elicited a prompt and marked increase in levels of transcripts for interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α, which are considered to be microglia/macrophage cytokines. The elevations preceded, or occurred concomitantly with, the rise in glial fibrillary acidic protein mRNA, an early manifestation of astrogliosis. In neonatal mice, IL-1 and TNF-α mRNA were elevated to a greater extent by an NC-implant injury, which produced astrogliosis, than after an NC-stab, with minimal astrogliosis. We determined whether endogenous interferon (IFN)-γ could be responsible for the observed increases in IL-1 and TNF-α, because IFN-γ is a potent microglia/macrophage activator, and because its exogenous administration to rodents enhanced astrogliosis after adult or neonatal insults. A lack of requirement for endogenous IFN-γ was demonstrated by three lines of evidence. First, no increase in IFN-γ transcripts could be found at injury. Second, the administration of a neutralizing antibody to IFN-γ did not attenuate astrogliosis. Third, in IFN-γ knockout adult mice, astrogliosis and increases in levels of IL-1α and TNF-α were induced rapidly by injury. The marked elevation of inflammatory cytokines is discussed in the context of astrogliosis and general CNS recovery.

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Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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“…[8][9][10]21,23) bFGF production increases under certain pathological conditions 9) and may prevent neuronal injury. A number of studies have shown the protective effect of bFGF in cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…5) Subsequent in vivo studies have shown that bFGF increased cortical blood flow 19) or dilated pial arterioles 20) and rat basilar arteries, 15) suggesting that bFGF may contribute to the regulation of pial microcirculation 19,20) and the cerebral posterior circulation. 15) bFGF is found constitutively in neurons and astroglia [8][9][10] with receptors found in cerebral blood vessels, 26) suggesting that bFGF may contribute to cerebrovascular regulation. 20) bFGF is of clinical interest because of its ability to reduce cerebral infarction.…”

Section: Introductionmentioning

confidence: 99%

Vasodilatory Effect of Basic Fibroblast Growth Factor in Isolated Rat Cerebral Arterioles: Mechanisms Involving Nitric Oxide and Membrane Hyperpolarization.

Kajita

Takayasu²,

Yoshida³

et al. 2001

Neurol. Med. Chir.(Tokyo)

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Basic fibroblast growth factor (bFGF), a potent mitogen, acutely dilates cerebral blood vessels and may be effective in reducing cerebral infarction. However, the vasodilatory mechanism, which may involve nitric oxide (NO), is not completely understood. This study investigated whether membrane hyperpolarization is also involved in this mechanism. Membrane potential (MP) of smooth muscle cells and vessel diameter of isolated intracerebral arterioles were simultaneously measured following extraluminal application of bFGF in rats. The involvement of NO and adenosine triphosphate-sensitive potassium (K ATP ) channels in bFGF-induced vasodilation and membrane hyperpolarization was evaluated using specific inhibitors, N G -monomethyl-L-arginine (L-NMMA, 10 -4 M) and glibenclamide (GB, 10 -5 M), respectively. The resting MP was recorded at a mean value of -31.9 ± 4.5 mV. bFGF (1 to 1000 ng/ml) produced significant vasodilation and hyperpolarization. Treatment with L-NMMA caused vasoconstriction and significantly attenuated bFGF-induced vasodilation without affecting membrane hyperpolarization. In the presence of GB, the membrane potential was significantly depolarized but the vessel diameter was only marginally reduced, so bFGF-induced membrane hyperpolarization was inhibited while arteriolar dilation was attenuated. These results suggest that bFGF-induced vasodilation is mediated by a mechanism involving both NO and membrane hyperpolarization, and that membrane hyperpolarization is caused by the activation of K ATP channels.

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“…In vitro, bFGF promotes the survival and out growth of a wide variety of neurons from embryonic rat brain and supports the survival and proliferation of brain glia and capillary endothelial cells (Gospo darowicz et al, 1986a;Pettman et al, 1985; Wa licke, 1988). In the intact brain, bFGF is localized to neurons and glial cells, whereas the high-affinity bFGF receptor (fig) is widely localized on both neu rons as well as non-neuronal cells (Emoto et al, 1989;Finklestein et al, 1988;Gomez-Pinilla et al, 1992;Woodward et al, 1992). In particular, the density of bFGF receptors is high in vascular brain structures (including circum ventricular organs and choroid plexus), most likely due to their localization Abbreviations used: ANOVA, analysis of variance; bFGF, ba sic fibroblast growth factor; BSA, bovine serum albumin; CGRP, calcitonin gene-related peptide; EAA, excitatory amino acids; L-NAME, ,vo-nitro-L-arginine methyl ester; PBS, phosphate buffered saline.…”

mentioning

confidence: 99%

“…Levels of bFGF rise in brain during development and after brain injury or stroke, suggesting a role for this factor in neural outgrowth and glial and vascu lar proliferation ("angiogenesis") occurring during these processes (Caday et al, 1990;Finklestein et al, 1988;Finklestein et al, 1990a,b). However, the precise role of bFGF in the mature intact brain re mains unknown.…”

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confidence: 99%

Basic Fibroblast Growth Factor Dilates Rat Pial Arterioles

Rosenblatt

Irikura

Caday

et al. 1994

J Cereb Blood Flow Metab

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Summary: Basic fibroblast growth factor (bFGF) is a polypeptide that promotes the survival and differentiation of brain neurons, glia, and endothelial cells. It has been shown recently that intravenously administered bFGF lowers blood pressure by systemic vasodilation; this ef fect is mediated, in part, by nitric oxide (NO)-dependent mechanisms. In the current study, we directly evaluated the effect of bFGF on pial arterioles of pentobarbital anesthetized Sprague-Dawley rats (n = 18) using the closed cranial window technique. Basic FGF (5-200 ng/ ml) produced dose-dependent vasodilation; maximal ves sel diameter (-120% of control) was reached at 100 ng/ Basic fibroblast growth factor (bFGF) is an 18-kDa polypeptide found within the mammalian brain with potent multipotential trophic effects on brain cells. In vitro, bFGF promotes the survival and out growth of a wide variety of neurons from embryonic rat brain and supports the survival and proliferation of brain glia and capillary endothelial cells (Gospo darowicz et al., 1986a;Pettman et al., 1985; Wa licke, 1988). In the intact brain, bFGF is localized to neurons and glial cells, whereas the high-affinity bFGF receptor (fig) is widely localized on both neu rons as well as non-neuronal cells (Emoto et al., 1989;Finklestein et al., 1988;Gomez-Pinilla et al., 1992;Woodward et al., 1992). In particular, the density of bFGF receptors is high in vascular brain structures (including circum ventricular organs and choroid plexus), most likely due to their localization Abbreviations used: ANOVA, analysis of variance; bFGF, ba sic fibroblast growth factor; BSA, bovine serum albumin; CGRP, calcitonin gene-related peptide; EAA, excitatory amino acids; L-NAME, ,vo-nitro-L-arginine methyl ester; PBS, phosphate buffered saline. 70ml. No vasodilation was found when bFGF was heat in activated, or preincubated with blocking antibody. Moreover, bFGF-induced vasodilation was attenuated by coadministration of the NO synthase inhibitor �-nitro L-arginine methyl ester (L-NAME), consistent with an NO-dependent mechanism. These results suggest that bFGF may play an important role in the regulation of cerebrovascular tone and cerebral blood flow.

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Increased basic fibroblast growth factor (bFGF) immunoreactivity at the site of focal brain wounds

Cited by 370 publications

References 25 publications

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

Vasodilatory Effect of Basic Fibroblast Growth Factor in Isolated Rat Cerebral Arterioles: Mechanisms Involving Nitric Oxide and Membrane Hyperpolarization.

Basic Fibroblast Growth Factor Dilates Rat Pial Arterioles

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