Fibroblast growth factors (FGF-1, FGF-2) promote migration and neurite growth of mouse cochlear ganglion cells in vitro: Immunohistochemistry and antibody perturbation

Hossain, Waheeda A.; Morest, D. Kent

doi:10.1002/1097-4547(20001001)62:1<40::aid-jnr5>3.0.co;2-l

Cited by 75 publications

(39 citation statements)

References 42 publications

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“…The combination of BDNF and ciliary neurotrophic factor (CNTF) enhanced auditory nerve survival even at delays of up to 6 weeks post-deafening (Yamagata et al, 2004). Consistent with an important role for FGF 1 in neurite outgrowth in the immature auditory system (Dazert et al, 1998;Hossain and Morest, 2000), we recently demonstrated the efficacy of BDNF plus FGF 1 in promoting systematic regrowth of the peripheral process of the auditory nerve even after a 6-week period of deafening (Miller et al, 2003b;2006a). Together, these results suggest post-noise treatment with NTF may prevent neural degeneration that occurs consequent to noise-induced sensory cell death.…”

Section: Growth Factorsmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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Section: Growth Factorsmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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“…Günümüze kadar FGF ailesine mensup 23 üye tespit edilmiş olup bunların varlığı omurgalı ve omurgasız birçok canlıda gösterilmiş-tir (3). FGF'ler embriyonik ve fetal gelişimde, damarlanma, yara iyileşmesi, doku oluşumu, yangı, sinirsel koruma, hücre çoğalması, hücre farklılaşması, hücre göçü, tümör gelişimi ve apoptosis gibi birçok önemli biyolojik sürecin düzenlenmesin-de rol almaktadır (4)(5)(6). FGF'ler heparin ve diğer anyonik moleküllere sıkıca bağlanan polipeptit ailesidir.…”

Section: Introductionunclassified

“…FGF'ler biyolojik aktivitelerini Fibroblast Growth Factor Receptör (FGFR) ile gerçekleştirir. Şimdiye kadar 4 adet FGFR (FGFR-1, FGFR-2, FGFR-3 ve FGFR-4) tespit edilmiştir (5).…”

Section: Introductionunclassified

“…Deneysel çalışmalarda FGF'lerin in vivo ve in vitro kültür ortamlarında bloke edilmesi çeşitli gelişim bozukluklarına neden olmaktadır (5). Bu çalışmadaki amacımız embriyo kültür ortamına farklı dozlarda anti-FGF-9 ilave ederek FGF-9'un aktivitesini ortadan kaldırmak suretiyle embriyoda meydana gelebilecek gelişim bozukluklarını ortaya koymaktır.…”

Section: Introductionunclassified

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The Effects Of Fgf-9 On In Vitro Embryonic Development

Tekinarslan¹,

Unur²,

Ülger³

et al. 2009

TUTFD

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“…During development of the otocyst the auditory and vestibular neuroblasts are amongst the first cell types to be specified (Hemond and Morest, 1991;Hossain and Morest, 2000;Fekete and Wu, 2002). They migrate from the prospective neural-sensorial domain epithelium at E9.5-10.5, simultaneously down-regulating epithelial cytokeratin.…”

Section: Bhlh Transcription Factorsmentioning

confidence: 99%

A network of growth and transcription factors controls neuronal differentation and survival in the developing ear

Sánchez-Calderón¹,

Milo²,

León³

et al. 2007

Int. J. Dev. Biol.

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Inner ear neurons develop from the otic placode and connect hair cells with central neurons in auditory brain stem nuclei. Otic neurogenesis is a developmental process which can be separated into different cellular states that are characterized by a distinct combination of molecular markers. Neurogenesis is highly regulated by a network of extrinsic and intrinsic factors, whose participation in auditory neurogenesis is discussed. Trophic factors include the fibroblast growth factor, neurotrophins and insulin-like peptide families. The expression domains of transcription factor families and their roles in the regulation of intracellular signaling pathways associated with neurogenesis are also discussed. Understanding and defining the key factors and gene networks in the development and function of the inner ear represents an important step towards defeating deafness. KEY WORDS: otic neurogenesis, IGF-I, FGF, inner ear, auditory ganglion, cochlear microarray Otic neurogenesisThe inner ear develops from the otic placode, an ectodermal patch located close to the neural tube that invaginates to form a transitory structure, the otic cup. This cup subsequently closes and pinches off from the ectoderm to generate the otic vesicle ( Figure 1). The otic vesicle is an autonomous structure that contains the information required to generate most of the cell types and structures of the adult inner ear (Bissonnette and Fekete, 1996;Bever et al., 2003; reviewed in Varela-Nieto et al., 2004). The mammalian inner ear is composed of six distinct sensory organs: the three cristae of the semicircular canal, the two maculae of the saccule and utricle and the organ of Corti in the cochlea. The cristae and the maculae are vestibular organs, whereas the organ of Corti is the organ of hearing (reviewed in Moller, 2006). The inner ear cochlear ganglion is formed by bipolar neurons that connect the peripheral sensory receptors or hair cells with central neurons in auditory brain stem nuclei. The correct organogenesis of the inner ear involves a dynamic balance of cell proliferation, differentiation, survival and death, processes that are tightly regulated by a network of extrinsic and intrinsic factors (Frago et al., 2000;Varela-Nieto et al., 2003 andLeon et al., 2004).The process of otic neurogenesis can be separated into different cellular states, each characterized by a distinct combination of molecular markers (summarized in Figure 1A). The first Int. J. Dev. Biol. 51: 557-570 (2007) doi: 10.1387/ijdb.072373hs visible output of otic neurogenesis is the delamination of neural cells (otic neuroblasts) from the otic cup (Fig. 1B). These neuroblasts are committed to generate otic neurons and they populate the cochleo-vestibular ganglion (CVG). This ganglion is generated from a region of the otic vesicle epithelium denominated the prospective neural-sensorial domain and that is defined by the domain in which Ngn1 and Deltal1 are co-expressed at early stages (Adam et al., 1998;Abu-Elmagd et al., 2001). It is believed that both n...

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Fibroblast growth factors (FGF-1, FGF-2) promote migration and neurite growth of mouse cochlear ganglion cells in vitro: Immunohistochemistry and antibody perturbation

Cited by 75 publications

References 42 publications

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

The Effects Of Fgf-9 On In Vitro Embryonic Development

A network of growth and transcription factors controls neuronal differentation and survival in the developing ear

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