Basic fibroblast growth factor applied to the optic nerve after injury increases long-term cell survival in the frog retina

Blanco, Rosa; López‐Roca, Argelio; Soto, Jorge; Blagburn, Jonathan M.

doi:10.1002/1096-9861(20000807)423:4<646::aid-cne9>3.0.co;2-u

Cited by 41 publications

(51 citation statements)

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“…Several animal studies have indicated that the application of bFGF could possiblely promote the survival of RGCs, and stimulates regrowth of the axons within the injured optic nerve [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

Positive Effects of bFGF Modified Rat Amniotic Epithelial Cells Transplantation on Transected Rat Optic Nerve

et al. 2015

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PurposeEffective therapy for visual loss caused by optic nerve injury or diseases has not been achieved even though the optic nerve has the regeneration potential after injury. This study was designed to modify amniotic epithelial cells (AECs) with basic fibroblast growth factor (bFGF) gene, preliminarily investigating its effect on transected optic nerve.MethodsA human bFGF gene segment was delivered into rat AECs (AECs/hbFGF) by lentiviral vector, and the gene expression was examined by RT-PCR and ELISA. The AECs/hbFGF and untransfected rat AECs were transplanted into the transected site of the rat optic nerve. At 28 days post transplantation, the survival and migration of the transplanted cells was observed by tracking labeled cells; meanwhile retinal ganglion cells (RGCs) were observed and counted by employing biotin dextran amine (BDA) and Nissl staining. Furthermore, the expression of growth associated protein 43 (GAP-43) within the injury site was examined with immunohistochemical staining.ResultsThe AECs/hbFGF was proven to express bFGF gene and secrete bFGF peptide. Both AECs/hbFGF and AECs could survive and migrate after transplantation. RGCs counting implicated that RGCs numbers of the cell transplantation groups were significantly higher than that of the control group, and the AECs/hbFGF group was significantly higher than that of the AECs group. Moreover GAP-43 integral optical density value in the control group was significantly lower than that of the cell transplantation groups, and the value in the AECs/hbFGF group was significantly higher than that of the AECs group.ConclusionsAECs modified with bFGF could reduce RGCs loss and promote expression of GAP-43 in the rat optic nerve transected model, facilitating the process of neural restoration following injury.

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Section: Introductionmentioning

confidence: 99%

Positive Effects of bFGF Modified Rat Amniotic Epithelial Cells Transplantation on Transected Rat Optic Nerve

et al. 2015

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“…Application of these factors, and the activation of their intracellular pathways, promotes the survival and axonal regeneration of axotomized RGCs (Blanco et al, 2008, 2000; Ríos-Muñoz et al, 2005; Soto et al, 2006b; Vega-Meléndez et al, 2014). All-trans retinoic acid (ATRA) is an important morphogen that controls the patterning and differentiation of neurons during development, and it has also been identified as a signaling molecule and transcriptional activator that regulates the expression of target genes, including those of growth factors and their receptors (Arrieta et al, 2005; Hernández-Pedro et al, 2008; Katsuki et al, 2009; Kurauchi et al, 2011; Qi et al, 2015; Wang and Halvorsen, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…The frog visual system is similar to the mammal's in that many of its RGCs die after axotomy (Blanco et al, 2000), but like that of the fish in that the surviving RGCs are able to regenerate and reconnect with their targets in the optic tectum (Soto et al, 2006a, 2003). Both the survival rate, and regeneration speed, of the frog's RGCs can be augmented by application of growth factors to optic nerve or eyeball, and we have studied the molecular pathways involved (Blanco et al, 2008, 2000; Ríos-Muñoz et al, 2005; Soto et al, 2006b; Vega-Meléndez et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Both the survival rate, and regeneration speed, of the frog's RGCs can be augmented by application of growth factors to optic nerve or eyeball, and we have studied the molecular pathways involved (Blanco et al, 2008, 2000; Ríos-Muñoz et al, 2005; Soto et al, 2006b; Vega-Meléndez et al, 2014). In view of its potential importance in RGC regeneration, the question arises as to whether RA signaling is present in the adult frog visual system, and whether axotomy causes its upregulation (as in fish) or not (as in mammals).…”

Section: Introductionmentioning

confidence: 99%

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Optic nerve injury upregulates retinoic acid signaling in the adult frog visual system

Duprey‐Díaz

Blagburn

Blanco

2016

Journal of Chemical Neuroanatomy

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Retinoic acid (RA) is important during development, in neuronal plasticity, and also in peripheral nervous system regeneration. Here we use the frog visual system as a model to investigate the changes in RA signaling that take place after axonal injury to the central nervous system. Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARα, β and (, and finally the catabolic enzyme CYP26A1. The levels of these proteins were quantified in extracts of retina and tectum using Western blotting. Animals were studied at 1 week, 3 weeks and 6 weeks after optic nerve transection. At the latter time point the RGC axons were re-entering the optic tectum. All the components of RA signaling were present at low to moderate levels in retinas and tecta of control, unoperated animals. In retina, soon after optic nerve injury there was a large increase in RALDH, some increase in the CRABPs, and a large increase in RGC RARβ and ( expression. These increases continued as the RGC axons were regenerating, with the addition of later RARα expression at 6 weeks. At no stage did CYP26A1 expression significantly change. In the tectum the levels of RALDH increased after axotomy and during regrowth of axons (3 weeks), then decreased at 6 weeks, at which time the levels of CYP26A1 increased. Axotomy did not cause an immediate increase in tectal RAR levels but RARα and RARβ increased after 3 weeks and RAR( only after 6 weeks. These results are consistent with RA signaling playing an important role in the survival and regeneration of frog RGCs.

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“…Basic fibroblast growth factor (bFGF) is a member of the FGF family that has been shown to protect neurons against injury and degeneration 5) . bFGF increases long-term cell survival in frog retinal ganglion cells after optic nerve axotomy 6) . In vitro actions of bFGF on mesenchymal and neuroectodermal cells include induction of or increase in proliferation, mitogenesis in glial cells, the support of neuronal survival, the promotion of neurite outgrowth 7,8) , morphological changes, anchorage-independent growth, differentiation, delayed senescence, angiogenesis, neovascularization, tissue differentiation, regulation of tissue specific functions 9) , wound healing 10) , other regenerative processes, abnormal cell differentiation and growth 9) .…”

Section: Introductionmentioning

confidence: 99%

bFGF Upregulates the Expression of NGFR in PC12 Cells

Shimosaka

Bhawal

2013

J. Hard Tissue Biology.

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The reciprocal and highly regulated processes of cellular proliferation, cellular differentiation, and progression to a postmitotic state during embryogenesis generate the cellular diversity in the developing nervous system. Growth factors, in part, can regulate these proliferative or differentiation processes by analogous mechanisms. Basic fibroblast growth factor (bFGF), a member of FGF family, has broad biological functions involving the regulation of cell growth, differentiation, and proliferation. As extension and remodeling of neurites play essential roles in development and neuronal plasticity, we investigated a role for nerve growth factor receptor (NGFR) on bFGF-induced neurite outgrowth in rat pheochromocytoma cell line, PC12. Our goal in the present study was to determine if there is a causal link between bFGF and NGFR. Results of these studies indicate that bFGF is required for NGFR-induced changes in morphology and transcriptional induction of the gene. We have provided convincing evidence that inhibitor of bFGF, PD173074, completely inhibited NGFR protein expression, whereas it partially blocked the NGFR protein expression in response to bFGF in PC12 cells. Another important finding of our study provides the data on the involvement of bFGF in MAPKdependent signaling pathways and neurite outgrowth in PC12 cells, which suggests a central role of MAPK in the neuronal induction by bFGF. Taken together, these results raise the possibility that bFGF activates a MAPKmediated pathway related to NGFR expression.

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Basic fibroblast growth factor applied to the optic nerve after injury increases long-term cell survival in the frog retina

Cited by 41 publications

References 59 publications

Positive Effects of bFGF Modified Rat Amniotic Epithelial Cells Transplantation on Transected Rat Optic Nerve

Positive Effects of bFGF Modified Rat Amniotic Epithelial Cells Transplantation on Transected Rat Optic Nerve

Optic nerve injury upregulates retinoic acid signaling in the adult frog visual system

bFGF Upregulates the Expression of NGFR in PC12 Cells

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