The combination of IGF1 and FGF2 and the induction of excessive ocular growth and extreme myopia

Ritchey, Eric R; Zelinka, Christopher; Tang, Junhua; Liu, Jun; Fischer, Andy J.

doi:10.1016/j.exer.2012.03.019

Cited by 60 publications

(60 citation statements)

References 54 publications

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“…Surprisingly, intravitreal injection of IGF-1 did not stimulate MG proliferation in the uninjured retina (Figure 2I, top panel). This result was reminiscent of that found in the post natal chick retina where Igf-1 collaborates with Fgf signaling to stimulate MG proliferation (Ritchey et al, 2012). …”

Section: Resultssupporting

confidence: 70%

“…We speculate that factors released from injured cells, like TNFα (Nelson et al, 2013), stimulate growth factor and cytokine induction in MG at the injury site where they act in an autocrine and/or paracrine fashion to drive MG reprogramming and proliferation. Interestingly, Insulin, IGF-1 and FGF-2 stimulate MG proliferation in the postnatal chick retina (Fischer et al, 2002; Ritchey et al, 2012). However, these cells rarely survive and make new neurons; perhaps reflecting differences in growth factor-regulated signaling cascades between fish and birds.…”

Section: Discussionmentioning

confidence: 99%

“…We were intrigued by reports that MG in the postnatal chick retina could be induced to proliferate in response to intravitreal injection of insulin/FGF2 or IGF-1/FGF2 (Fischer et al, 2002; Fischer and Reh, 2002; Ritchey et al, 2012). Although these treatments stimulate MG proliferation in the chick retina, rarely do these cells survive and regenerate neurons.…”

Section: Introductionmentioning

confidence: 99%

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Retinal Injury, Growth Factors, and Cytokines Converge on β-Catenin and pStat3 Signaling to Stimulate Retina Regeneration

et al. 2014

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Summary Müller glia (MG) in the zebrafish retina respond to retinal injury by generating multipotent progenitors for retinal repair. Here we show that Insulin, Igf-1 and FGF signaling components are necessary for retina regeneration. Interestingly, these factors synergize with each other and with HB-EGF and cytokines to stimulate MG to generate multipotent progenitors in the uninjured retina. These factors act by stimulating a core set of signaling cascades (Mapk/Erk, PI3K, β-catenin and pStat3) that are also shared with retinal injury and exhibit a remarkable amount of crosstalk. Our studies suggest that MG are both the producers and responders of factors that stimulate MG reprogramming and proliferation following retinal injury. The identification of a core set of regeneration-associated signaling pathways required for MG reprogramming not only furthers our understanding of retina regeneration in fish, but also suggests new targets for enhancing regeneration in mammals.

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Section: Resultssupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Retinal Injury, Growth Factors, and Cytokines Converge on β-Catenin and pStat3 Signaling to Stimulate Retina Regeneration

et al. 2014

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“…Further, in combination, insulin/IGF1 and FGF2 act synergistically to stimulate the formation of MGPCs in chick and zebrafish retinas (Ritchey et al, 2012;Wan et al, 2014). We tested whether a single injection of FGF2, IGF1 or insulin activates mTor signaling.…”

Section: Inhibition Of Mtormentioning

confidence: 99%

mTor-signaling is required for the formation of proliferating Müller glia-derived progenitor cells in the chick retina

et al. 2016

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We investigate the roles of mTor signaling in the formation of Müller glia-derived progenitor cells (MGPCs) in the chick retina. During embryonic development, pS6 (a readout of active mTor signaling) is present in early-stage retinal progenitors, differentiating amacrine and ganglion cells, and late-stage progenitors or maturing Müller glia. By contrast, pS6 is present at low levels in a few scattered cell types in mature, healthy retina. Following retinal damage, in which MGPCs are known to form, mTor signaling is rapidly activated in Müller glia. Inhibition of mTor in damaged retinas prevented the accumulation of pS6 in Müller glia and reduced numbers of proliferating MGPCs. Inhibition of mTor had no effect on MAPK signaling or on upregulation of the stem cell factor Klf4, whereas Pax6 upregulation was significantly reduced. Inhibition of mTor potently blocked the MGPC-promoting effects of Hedgehog, Wnt and glucocorticoid signaling in damaged retinas. In the absence of retinal damage, insulin, IGF1 and FGF2 induced pS6 in Müller glia, and this was blocked by mTor inhibitor. In FGF2-treated retinas, in which MGPCs are known to form, inhibition of mTor blocked the accumulation of pS6, the upregulation of Pax6 and the formation of proliferating MGPCs. We conclude that mTor signaling is required, but not sufficient, to stimulate Müller glia to give rise to proliferating progenitors, and the network of signaling pathways that drive the formation of MGPCs requires activation of mTor.

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“…Transient myopia can also be caused by other drugs such as promethazine hydrochloride (Phenergan) [52], prochlorperazine (Compazine) [53], insulin [54][55][56][57], IGF1 and FGF2 [58], antithrombotic [59], opiate [60], tetracycline [15,61], aripiprazole [62,63], amisulpride [64], oseltamivir [65], mefenamic acid [66], ectasy [67], phendimetrazine and ephedrine used as anorexiants [68], equine antilymphocyte globulins [69], metronidazole [70], aspirine and deturgylone [71,72], isotretinoin (accutane) [3], isosorbide dinitrate [74], quinine [75].…”

mentioning

confidence: 99%

Transient Drug-Induced Myopia

Dkw¹

2014

SAJ Case Reports

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Myopia is the most common eye disease and is one of the leading causes of vision impairment worldwide [1,2]. Prevalence of myopia is significantly different among racial groups, although its worldwide prevalence is approximately 30% (3%-84%) [3]. The highest prevalence is found in East Asia, such as mainland China [3]. The prevalence of myopia in the US population was estimated in the early 1970s to be 25% in persons aged 12 to 54 years [4]. A recent meta-analysis of population-based studies found a prevalence of 25% in persons over age 40 [5].Myopia (nearsightedness) is a refractive error, a condition in which the cornea and lens of the nonaccommoding eye have too much plus power for the length of eye. As a result, images of distant objects are focused in front of the retina and thus appear blurred.Myopia has been recognized as a distinct visual disability for millennia and has been known for more than 2000 years and was first described by the ancient Greeks [6,7]. It was probably the ancient Greeks who coined the term, using the roots myein (to close) and ops (eye) to characterize those individuals who narrow their eyelids to improve distance visual acuity, the pinhole effect. The focus of distant parallel rays of light falls anterior to the retinal plane and produces a blurred image in myopia. This situation can arise because either the primary refractive components are too powerful or the globe is too long. Thus, myopia can be due to increased corneal or lenticular curvature, or an increase in the lens index of refraction, as occurs with the development of nuclear sclerosis. More commonly, myopia is the result of axial elongation of the posterior segment of the eye.Transient drug-induced myopia is a myopia induced by a drug as a transient side effect. A side effect (adverse drug reaction) is basically an unintended, unwanted occurrence that results from taking a drug. An adverse drug reaction is an expression that describes harm associated with the use of given medication at a normal dosage during normal use. Adverse drug reactions may occur following a single dose or prolonged administration of a drug or result from the combination of two or more drugs [8]. All drugs that come in the market may cause side effects, where many are minor and few are serious. Myopia (nearsightedness) is a refractive error, a condition in which the cornea and lens of the nonaccommoding eye have too much plus power for the length of eye. As a result, images of distant objects are focused in front of the retina and thus appear blurred. Transient drug-induced myopia is a myopia induced by a drug as a transient side effect. Several case reports of transient drug-induced myopia have been reported. These cases have been associated with secondary angle closure glaucoma and other ocular conditions such as choroidal detachment, maculopathy, retinal folds. Drugs known to produce this effect include sulfa drugs and other medications. The possible mechanism is thought to be an allergic reaction to the drug. Both ciliary muscle contraction a...

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The combination of IGF1 and FGF2 and the induction of excessive ocular growth and extreme myopia

Cited by 60 publications

References 54 publications

Retinal Injury, Growth Factors, and Cytokines Converge on β-Catenin and pStat3 Signaling to Stimulate Retina Regeneration

Retinal Injury, Growth Factors, and Cytokines Converge on β-Catenin and pStat3 Signaling to Stimulate Retina Regeneration

mTor-signaling is required for the formation of proliferating Müller glia-derived progenitor cells in the chick retina

Transient Drug-Induced Myopia

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