Immunohistochemical localization of basic fibroblast growth factor in cultured rat astrocytes and oligodendrocytes

Vijayan, Vijaya K.; Lee, Y.L.; Eng, Lawrence F.

doi:10.1016/0736-5748(93)90084-q

Cited by 24 publications

(23 citation statements)

References 51 publications

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“…At least four amino terminus extended isoforms of FGF-2 arise from the same gene due to initiation of translation at di erent start codons with di erent cells expressing di erent isoforms (Florkiewicz and Sommer, 1989). All FGF-2 isoforms are detected in both the cytoplasm and the nucleus of expressing cells (Powell and Klagsbrun, 1991;Florkiewicz et al, 1991;Gualandris et al, 1993;Woodward et al, 1992;Vijayan et al, 1993;Stachowiak et al, 1994Stachowiak et al, , 1996a. Nuclear presence of FGF-2 was detected in rat brain astrocytes both in vivo (Woodward et al, 1992) and in vitro (Vijayan et al, 1993) and in cultured human astrocytes and glioma cells (Mo ett et al, 1996;Stachowiak et al, 1996a).…”

Section: Introductionmentioning

confidence: 99%

“…All FGF-2 isoforms are detected in both the cytoplasm and the nucleus of expressing cells (Powell and Klagsbrun, 1991;Florkiewicz et al, 1991;Gualandris et al, 1993;Woodward et al, 1992;Vijayan et al, 1993;Stachowiak et al, 1994Stachowiak et al, , 1996a. Nuclear presence of FGF-2 was detected in rat brain astrocytes both in vivo (Woodward et al, 1992) and in vitro (Vijayan et al, 1993) and in cultured human astrocytes and glioma cells (Mo ett et al, 1996;Stachowiak et al, 1996a). With the observation that FGF-2 remains cell associated and may not be secreted by a classical mechanism, a regulated targeting of endogenous FGF-2 to the nucleus (Puchacz et al, 1993;Stachowiak et al, 1994Stachowiak et al, , 1996bMo ett et al, 1994Mo ett et al, , 1996 suggests that this growth factor may serve as an intracrine signaling molecule.…”

Section: Introductionmentioning

confidence: 99%

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Nuclear accumulation of FGF-2 is associated with proliferation of human astrocytes and glioma cells

et al. 1997

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FGF-2 has been implicated in the neoplastic transformation of glioma cells and in the transition of normal quiescent astrocytes to a proliferating, reactive state. In the present study we have observed that in human glial cells, levels and subcellular localization of FGF-2 are di erent in quiescent and proliferating cells. FGF-2 was detected in the cytoplasm of non-reactive astrocytes in human brain sections. In contrast FGF-2 was located within the cytoplasm and nuclei of reactive astrocytes in gliotic brain tissue and in neoplastic cells of glioma tumors. In vitro, FGF-2 was found predominantly in the nucleus of subcon¯uent proliferating astrocytes, but was detected only in the cytoplasm of density arrested quiescent astrocytes. Our results suggest that reduced cell contact stimulates nuclear accumulation of FGF-2, accompanying mitotic activation of reactive human astrocytes. FGF-2 was constitutively localized to the nucleus of continuously proliferating glioma cells independent of cell density. A role for intracellular FGF-2 was further suggested by the observation that glioma cells that are not stimulated to proliferate by extracellular FGF-2 proliferated faster when transfected with FGF-2 expressing vectors. This increased proliferation correlated with nuclear accumulation of FGF-2. Cell proliferation was attenuated by 5'-deoxy-5'-methylthioadenosine, a FGF-2 receptor tyrosine kinase inhibitor that acts within the cell, but was una ected by myo-inositol hexakis [dihydrogen phosphate] that disrupts FGF-2 binding to plasma membrane receptors. Our results indicate that FGF-2 serves as a nuclear regulator of proliferation in astrocytic cells. In glioma cells, the constitutive presence of FGF-2 in the nucleus may promote proliferation that is insensitive to cell contact inhibition.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nuclear accumulation of FGF-2 is associated with proliferation of human astrocytes and glioma cells

et al. 1997

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“…Release of FGF-1 and 2 may occur through leakage from damaged cells or from viable cells through a novel mechanism (Mignatti et al, 1992;Cao and Pettersson, 1993). FGF-1 and 2 have both been reported to show nuclear as well as cytoplasmic localisation (Cao and Pettersson, 1993;Vijayan et al, 1993).…”

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confidence: 99%

Expression of fibroblast growth factor 1 is lower in breast cancer than in the normal human breast

Bansal

Yiangou²,

Coope³

et al. 1995

Br J Cancer

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“…Rat brain sections were stained for select cytokines and growth factors in order to characterize the stab wound injury. The pattern of expression for tumor necrosis factor (TNF) a, interleukin 6 (IL6), transforming growth factor (TGF) p, and basic fibroblast growth factor (bFGF) following injury appeared to be as described previously (data not shown) (Finklestein et al, 1988;Woodroofe et al, 1991;Logan et al, 1992;Woodward et al, 1992;Vijayan et al, 1993;Taupin et al, 1993;O'Brien et al, 1994;Benveniste and Benos, 1995).…”

Section: General Observationsmentioning

confidence: 73%

Chemokine expression in rat stab wound brain injury

Ghirnikar

Lee

et al. 1996

J. Neurosci. Res.

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A traumatic injury to the adult mammalian central nervous system (CNS) results in reactive astrogliosis and the migration of hematogenous cells into the damaged neural tissue. Chemokines, a novel class of chemoattractant cytokines, are now being recognized as mediators of the inflammatory changes that occur following injury. The expression of MCP‐1 (macrophage chemotactic peptide‐1), a member of the β family of chemokines, has recently been demonstrated in trauma in the rat brain (Berman et al.: J Immunol 156:3017–3023, 1996). Using a stab wound model for mechanical injury, we studied the expression of two other β chemokines: RANTES (Regulated on Activation, Normal T cell Expressed and Secreted) and MIP‐1 β (macrophage inflammatory protein‐1 beta) in the rat brain. The stab wound injury was characterized by widespread gliosis and infiltration of hematogenous cells. Immunohistochemical staining revealed the presence of RANTES and MIP‐1 β in the injured brain. RANTES and MIP‐1 β were both diffusely expressed in the necrotic tissue and were detected as early as 1 day post‐injury (dpi). Double‐labeling studies showed that MIP‐1 β, but not RANTES, was expressed by reactive astrocytes near the lesion site. In addition, MIP‐1 β staining was also detected on macrophages at the site of injury. The initial expression of the chemokines closely correlated with the appearance of inflammatory cells in the injured CNS, suggesting that RANTES and MIP‐1 β may play a role in the inflammatory events of traumatic brain injury. This study also demonstrates for the first time MIP‐1 β expression in reactive astrocytes following trauma to the rat CNS. © 1996 Wiley‐Liss, Inc.

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Immunohistochemical localization of basic fibroblast growth factor in cultured rat astrocytes and oligodendrocytes

Cited by 24 publications

References 51 publications

Nuclear accumulation of FGF-2 is associated with proliferation of human astrocytes and glioma cells

Nuclear accumulation of FGF-2 is associated with proliferation of human astrocytes and glioma cells

Expression of fibroblast growth factor 1 is lower in breast cancer than in the normal human breast

Chemokine expression in rat stab wound brain injury

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