Expression of basic fibroblast growth factor isoforms in postmitotic sympathetic neurons: synthesis, intracellular localization and involvement in karyokinesis

Nindl, W; Kavakebi, Pujan; Claus, Piet; Grothe, Claudia; Pfaller, Kristian; Klimaschewski, Lars

doi:10.1016/j.neuroscience.2003.11.032

Cited by 22 publications

(15 citation statements)

References 41 publications

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“…Studies from stable cell lines, obtained on the basis of their ability to survive hi-FGF-2 overexpression, have proposed that hi-FGF-2 confers a transformed phenotype [10]. Studies using transient gene transfer on the other hand have shown that, unlike 18 kDa FGF-2, prolonged nuclear accumulation of hi-FGF-2 causes mitotic arrest, binucleation and eventually cell death in cardiomyocytes [53,59,60], HEK293 cells (our unpublished observations) and neuronal cells [61].…”

Section: Fgf-2mentioning

confidence: 70%

Fibroblast growth factor 2 isoforms and cardiac hypertrophy

Kardami

Jiang

Jimenez

et al. 2004

Cardiovascular Research

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Fibroblast growth factor 2 (FGF-2), a multifunctional polypeptide that affects cell growth and differentiation and becomes upregulated by stress, is expressed as AUG-initiated 18 kDa FGF-2 or CUG-initiated 21-34 kDa (hi-FGF-2) isoforms. Animal models have provided strong evidence that FGF-2 is essential for the manifestation of overload- and angiotensin-induced cardiac hypertrophy. Nevertheless, studies to-date have not discriminated between the activities of 18 kDa FGF-2 and hi-FGF-2. Our recent work has pointed to a potent pro-hypertrophic effect of added hi-FGF-2, and a pro-apoptotic effect of sustained intracrine hi-FGF-2 signaling. In the future, it will be important to differentiate between the activities of the different FGF-2 isoforms in the context of adaptive and maladaptive myocardial hypertrophy and heart failure. Based on all available evidence, we propose that while the 18-kDa FGF-2 is a component of an adaptive trophic response, a switch to hi-FGF-2 accumulation would exacerbate hypertrophy and contribute to cell death, thus driving the myocardium towards a maladaptive phenotype.

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Section: Fgf-2mentioning

confidence: 70%

Fibroblast growth factor 2 isoforms and cardiac hypertrophy

Kardami

Jiang

Jimenez

et al. 2004

Cardiovascular Research

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“…The investigation of HMW FGF-2 and their role(s) in the biological activity of PDGFs should also take into account that in certain cell types HMW FGF-2 has been unequivocally linked to growth inhibition [Quarto et al, 1991b;Dono et al, 1998;Nindl et al, 2004]. Further studies will be needed to understand the role(s) of nuclear accumulation of HMW FGF-2 in smooth muscle cells in vivo, and their effect(s) on the SMC functions involved in the vessel wall remodeling that characterizes a variety of vascular pathologies.…”

Section: Discussionmentioning

confidence: 99%

PDGF‐BB induces vascular smooth muscle cell expression of high molecular weight FGF‐2, which accumulates in the nucleus

Pintucci¹,

Yu²,

Saponara³

et al. 2005

J of Cellular Biochemistry

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Basic fibroblast growth factor (FGF-2) and platelet-derived growth factor (PDGF) are implicated in vascular remodeling secondary to injury. Both growth factors control vascular endothelial and smooth muscle cell proliferation, migration, and survival through overlapping intracellular signaling pathways. In vascular smooth muscle cells PDGF-BB induces FGF-2 expression. However, the effect of PDGF on the different forms of FGF-2 has not been elucidated. Here, we report that treatment of vascular aortic smooth muscle cells with PDGF-BB rapidly induces expression of 20.5 and 21 kDa, high molecular weight (HMW) FGF-2 that accumulates in the nucleus and nucleolus. Conversely, PDGF treatment has little or no effect on 18 kDa, low-molecular weight FGF-2 expression. PDGF-BB-induced upregulation of HMW FGF-2 expression is controlled by sustained activation of extracellular signal-regulated kinase (ERK)-1/2 and is abolished by actinomycin D. These data describe a novel interaction between PDGF-BB and FGF-2, and indicate that the nuclear forms of FGF-2 may mediate the effect of PDGF activity on vascular smooth muscle cells.

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“…In cultures of dissociated dopaminergic neurons obtained from rat mesencephalon at embryonic day 14, 18-kDa-FGF-2 supplemented to the medium accounts for significantly increased branching points of neurites, whereas, HMW-FGF-2 isoforms significantly enhanced neural soma areas (Grothe et al, 2000b). Furthermore, over-expressed HMW-FGF-2 seems to specifically affect karyokinesis in postmitotic peripheral and central neurons in culture (Nindl et al, 2004). The over-expression of the 18-kDa-FGF-2 isoform and HMW-FGF-2 in cultured PC 12 cells and in immortalized Schwann cells resulted in distinct altered cell morphology (Grothe et al, 1998).…”

Section: Differential Effects Of Fgf-2 Isoforms Were Also Seen In Othmentioning

confidence: 94%

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

Haastert

Lipokatic

Fischer

et al. 2006

Neurobiology of Disease

111

118

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Expression of basic fibroblast growth factor isoforms in postmitotic sympathetic neurons: synthesis, intracellular localization and involvement in karyokinesis

Cited by 22 publications

References 41 publications

Fibroblast growth factor 2 isoforms and cardiac hypertrophy

Fibroblast growth factor 2 isoforms and cardiac hypertrophy

PDGF‐BB induces vascular smooth muscle cell expression of high molecular weight FGF‐2, which accumulates in the nucleus

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

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