Acidic fibroblast growth factor stimulates opsin levels in retinal photoreceptor cells in vitro

Hicks, David; Courtois, Yves

doi:10.1016/0014-5793(88)80141-8

Cited by 59 publications

(19 citation statements)

References 13 publications

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“…A number of factors, in addition to RA, have been shown to promote rod photoreceptor cell differentiation in retinal cell cultures, including cilliary neurotrophic factor (18), acidic fibroblast growth factor (19), basic FGF (20), and taurine (21). It could be that expression of several of these factors is enhanced by RA in the retina as RA is known to induce the expression of several growth factors in various tissues.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid alters photoreceptor development in vivo

Hyatt

Schmitt

Fadool

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

200

184

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Application of exogenous retinoic acid (RA) to zebrafish during the initial stages of photoreceptor differentiation results in a precocious development of rod photoreceptors and an inhibition of cone photoreceptor maturation. The acceleration of rod differentiation is observed initially within the ventral retina 3 days after fertilization, following 24 hr of RA application, and within the dorsal retina 4 days after fertilization, following 48 hr of RA application. The differentiation of rods was impeded significantly when the synthesis of endogenous retinoic acid was inhibited by citral prior to the initial stage of rod differentiation. RA-treated embryos labeled for bromodeoxyuridine (BrdU) uptake revealed that RA exerts its effect on a postmitotic cell population within the developing retina. During normal development in zebrafish, rod differentiation is most robust within the ventral retina, a region previously shown to be rich in RA. Our data suggest that the RA signaling pathway is involved in the differentiation and maturation of both the rod and cone photoreceptors within the developing zebrafish retina.Recent experiments suggest that retinoic (vitamin A) acid (RA) plays an important role in early eye development. Application of an excess of RA to zebrafish embryos during the formation of the optic primordia-9.5-11.5 hr after fertilization (pf)-induces a proliferation of cells in the ventral part of the eye and the formation of a second retina (1). Inhibition of RA synthesis in the zebrafish eye at the same stage results in the formation of half-eyes that lack a ventral retina (2). A similar ocular phenotype is seen in embryonic mice in which RA receptors have been genetically eliminated via molecular manipulation (3). A study of the effects of RA on molecular markers expressed in early stages of zebrafish eye development indicates that RA exerts a ventralizing effect on the retina; i.e., it enhances ventral retinal characteristics while diminishing dorsal retinal features (4).In postnatal rat and embryonic chicken cell cultures, RA promotes the differentiation and survival of retinal photoreceptors, suggesting that RA may also play a role later in development, in photoreceptor differentiation (5, 6). The adult zebrafish retina contains rods and four classes of cones that can be distinguished morphologically (7). Short single cones are ultraviolet-sensitive, whereas long single cones are bluesensitive. The principal member of the double cone is redsensitive, whereas the accessory member is green-sensitive (8).Photoreceptors first develop at about 2 days pf in zebrafish in a patch of retina located ventrally (9). Subsequent photoreceptor differentiation in zebrafish is complex and does not occur uniformly across the retina (10, 11). Thus, distinct differences in the distribution and extent of maturation of rods and cones are observed in various retinal regions in zebrafish 3 days or older. In this study, we report the effects of RA on the early stages of photoreceptor cell differentiation in vivo.R...

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Section: Discussionmentioning

confidence: 99%

Retinoic acid alters photoreceptor development in vivo

Hyatt

Schmitt

Fadool

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

200

184

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“…As exogenous FGF are known to increase survival of neuronal cells such as photoreceptors (11,17,18), cholinergic neurons, and retinal ganglion cells (51), in view of our data, the survival activity of exogenous FGF should depend on an increase in the expression of FGF1 or FGF2 in these neuronal cells.…”

Section: Fig 9 Activation Of Erk1 By Fgf1 Fgfmentioning

confidence: 99%

“…These patterns of FGF expression suggest that these growth factors are involved in the integrity, development, and differentiation of the central nervous system. In fact, in vitro studies have shown that FGF1 promotes the survival of photoreceptors (11) and the neuritic outgrowth of dissociated retinal ganglion cells (12). FGF1 also inhibits pigmentation of immature pigmented epithelium cells of embryonic chick retina and stimulates ganglion cell differentiation (13).…”

Section: Fgf1mentioning

confidence: 99%

The Neurotrophic Activity of Fibroblast Growth Factor 1 (FGF1) Depends on Endogenous FGF1 Expression and Is Independent of the Mitogen-activated Protein Kinase Cascade Pathway

Renaud

Desset

Oliver

et al. 1996

Journal of Biological Chemistry

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The expression of fibroblast growth factor (FGF) 1, a potent neurotrophic factor, increases during differentiation and remains high in adult neuronal tissues. To examine the importance of this expression on the neuronal phenotype, we have used PC12 cells, a model to study FGF-induced neuronal differentiation. After demonstrating that FGF1 and FGF2 are synthesized by PC12 cells, we investigated if FGF1 expression could be a key element in differentiation. Using the cell signaling pathway to determine the effects of FGF1 alone, FGF1 plus heparin, or a mutated FGF1, we showed an activation to the same extent of mitogen-activated protein (MAP) kinase kinase and MAP kinase (extracellular regulated kinase 1). However, only FGF1 plus heparin could promote PC12 cell differentiation. Thus, the MAP kinase pathway is insufficient to promote differentiation. Analysis of the PC12 cells after the addition of FGF1 plus heparin or FGF2 demonstrated a significant increase in the level of FGF1 expression with the same time course as the appearance of the neuritic extensions. Transfection experiments were performed to enhance constitutivly or after dexamethasone induction the level of FGF1 expression. The degree of differentiation achieved by the cells correlated directly with the amount of FGF1 expressed. The MAP kinase pathway did not appear to be involved. Interestingly, a 5-fold increase in FGF1 in constitutive transfected cells extended dramatically their survival in serum-free medium, suggesting that the rise of FGF1 synthesis during neuronal differentiation is probably linked to their ability to survive in the adult. All of these data demonstrate that, in contrast to the MAP kinase cascade, FGF1 expression is sufficient to induce in PC12 cells both differentiation and survival. It also shows that auto-and trans-activation of FGF1 expression is involved in the differentiation process stimulated by exogenous FGFs through a new pathway which remains to be characterized. FGF11 and 2 are widely distributed in the peripheral and central nervous systems in the adult. In rat brain, FGF2 is present in most neurons within the cerebral cortex (1), hippocampus (2), and cerebellum (3). High levels of FGF1 expression have been observed in motor neurons, primary sensory neurons, and retinal ganglion neurons (4, 5). In chick brain, the expression of FGF1 is developmentally regulated (6). In bovine and rat embryonic retina, all neuronal layers express FGF1 with an appearance corresponding to their sequential differentiation (7, 8). In rat, the level of FGF1 expression remains uniformly low throughout the embryonic period until postnatal day 7. Thereafter, it increases rapidly, reaching a maximum in the adult retina. In the intermediate central nervous system, subclasses of FGF receptors appear to be down-regulated during development (9), and during retinal embryonic development, the expression of FGFR1 and FGFR2 follows the retinal layering (10). These patterns of FGF expression suggest that these growth factors are involved in the integrit...

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“…Surprisingly, BDNF reduced the incidence of macrophages from that seen in light-damaged retinas (Figs. 2C and 3C (17,20,21); aFGF (35) and bFGF (16) prolong photoreceptor survival in vitro; and BDNF (2, 7) and CNTF (36) Light damage is thought to result from the generation of oxygen free radicals and the ensuing peroxidation of lipids (37), and when viewed in the microscope, outer segments usually are the first part of the photoreceptor cell to exhibit damage (38,39). Preservation, by the injected factors, of some intact outer segments in most of the rescued retinas indicates that these agents actually protect the cells from damage at an early stage in the injury event.…”

Section: Quantification Of Photoreceptor Rescue and Macrophagementioning

confidence: 99%

Multiple growth factors, cytokines, and neurotrophins rescue photoreceptors from the damaging effects of constant light.

LaVail

Unoki

Yasumura

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

611

395

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Recent demonstrations ofsurvival-promoting activity by neurotrophic agents in diverse neuronal systems have raised the possibility of pharmacological therapy for inherited and degenerative disorders of the central nervous system. We have shown previously that, in the retina, basic fibroblast growth factor delays photoreceptor degeneration in Royal College ofSurgeons rats with inherited retinal dystrophy and that the growth factor reduces or prevents the rapid photoreceptor degeneration produced by constant light in the rat. This light-damage model now provides an efficient way to assess quantitatively the survival-promoting activity in Wivo of a number of growth factors and other molecules. We report here that photoreceptors can be significantly protected from the damaging effects of light by intravitreal injection of eight different growth factors, cytokines, and neurotrophins that typically act through several distinct receptor families. In addition to basic fibroblast growth factor, those factors providing a high degree of photoreceptor rescue include brainderived neurotrophic factor, ciliary neurotrophic factor, interleukin 1fl, and acidic fibroblast growth factor; those with less activity include neurotrophin 3, insulin-like growth factor II, and tumor necrosis factor a; those showing little or no protective effect are nerve growth factor, epidermal growth factor, platelet-derived growth factor, insulin, insulin-like growth factor I, heparin, and laminin. Although we used at least one relatively high concentration ofeach agent (the highest available), it is still possible that other concentrations or factor combinations might be more protective. Injecting heparin along with acidic fibroblast growth factor or basic fibroblast growth factor further enhanced the degree of photoreceptor survival and also suppressed the increased incidence of macrophages produced by either factor, especially basic fibroblast growth factor. These results now provide the impetus for determining the normal function in the retina, mechanism(s) of rescue, and therapeutic potential in human eye diseases for each agent.

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Acidic fibroblast growth factor stimulates opsin levels in retinal photoreceptor cells in vitro

Cited by 59 publications

References 13 publications

Retinoic acid alters photoreceptor development in vivo

Retinoic acid alters photoreceptor development in vivo

The Neurotrophic Activity of Fibroblast Growth Factor 1 (FGF1) Depends on Endogenous FGF1 Expression and Is Independent of the Mitogen-activated Protein Kinase Cascade Pathway

Multiple growth factors, cytokines, and neurotrophins rescue photoreceptors from the damaging effects of constant light.

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