Members of the BMP, Shh, and FGF morphogen families promote chicken statoacoustic ganglion neurite outgrowth and neuron survival <i>in vitro</i>

Fantetti, Kristen N.; Fekete, Donna M.

doi:10.1002/dneu.20988

Cited by 29 publications

(32 citation statements)

References 70 publications

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“…1A, G). Treatment with BMP4, an inducer of neuritogenesis in neurons (Fantetti and Fekete, 2012), induced neuritogenesis gradually by day 6 (Fig. 1E, G), although the effect was not as strong as that for NGFinduced neuritogenesis ( Fig.…”

Section: Resultsmentioning

confidence: 92%

“…BMPs bind to two classes of transmembrane receptors (Hogan, 1996) and activate two downstream pathways, the Smad and p38 MAPK signaling pathways (Heldin et al, 1997;Kimura et al, 2000). BMPs have also been shown to induce neurite outgrowth in PC12 cells and neurons (Fantetti and Fekete, 2012;Iwasaki et al, 1996). In the BMP-induced neuronal differentiation of PC12 cells, neuritogenesis is dependent upon BMP-mediated p38 MAPK signaling (Iwasaki et al, 1999;Yanagisawa et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Induction of Neuritogenesis in PC12 Cells by a Pulsed Electromagnetic Field via MEK-ERK1/2 Signaling

Kudo

Kanetaka

Shimizu

et al. 2013

Cell Struct. Funct.

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ABSTRACT. We examined the regulation of neuritogenesis by a pulsed electromagnetic field (PEMF) in rat PC12 pheochromocytoma cells, which can be induced to differentiate into neuron-like cells with elongated neurites by inducers such as nerve growth factor (NGF). Plated PC12 cells were exposed to a single PEMF (central magnetic flux density, 700 mT; frequency, 0.172 Hz) for up to 12 h per day and were then evaluated for extent of neuritogenesis or acetylcholine esterase (AChE) activity. To analyze the mechanism underlying the effect of the PEMF on the cells, its effects on intracellular signaling were examined using the ERK kinase (MEK) inhibitors PD098059 and U0126 (U0124 was used as a negative control for U0126). The number of neuritebearing PC12 cells and AChE activity increased after PEMF exposure without the addition of other inducers of neuritogenesis. Additionally, PEMF exposure induced sustained activation of ERK1/2 in PC12 cells, but not in NR8383 rat alveolar macrophages. Furthermore, U0126 strongly inhibited PEMF-dependent ERK1/2 activation and neuritogenesis. The PEMF-dependent neuritogenesis was also suppressed by PD098059, but not U0124. These results suggest that PEMF stimulation independently induced neuritogenesis and that activation of MEK-ERK1/2 signaling was induced by a cell-type-dependent mechanism required for PEMF-dependent neuritogenesis in PC12 cells.

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Section: Resultsmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Induction of Neuritogenesis in PC12 Cells by a Pulsed Electromagnetic Field via MEK-ERK1/2 Signaling

Kudo

Kanetaka

Shimizu

et al. 2013

Cell Struct. Funct.

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“…Nevertheless, several genes linked to cell motility showed level changes, such as RhoA, calcium signaling molecules (Wipf1,Rhpn1,Arpc4,Actc1,Rac3,Pak3,Casq2,Iptr3), and axon guidance molecules (Bdnf, Nrtk2, Sema3d; Table 3). Fgf19 and Bmp7, which promote statoacoustic ganglion outgrowth (Fantetti and Fekete, 2012), were upregulated (Table 3).…”

Section: Wnt9a-oe Induces Changes In Gene Expression By E6mentioning

confidence: 99%

“…The radial spread of axons is sustained on E18 and mirrored by presynaptic changes (ribbon counts), although the latter may be an independent phenomenon. Increased abneural projections may reflect Wnt9a-induced changes in molecules that stimulate auditory axon outgrowth: FGFs, BMP7, or survival neurotrophins (Garrido et al, 1998;Fantetti and Fekete, 2012). Such genes that are elevated upon Wnt9a-OE include Fgf3, Fgf19, and Bmp7.…”

mentioning

confidence: 99%

Wnt9a Can Influence Cell Fates and Neural Connectivity across the Radial Axis of the Developing Cochlea

Munnamalai¹,

Sienknecht

Duncan

et al. 2017

J. Neurosci.

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Vertebrate hearing organs manifest cellular asymmetries across the radial axis that underlie afferent versus efferent circuits between the inner ear and the brain. Therefore, understanding the molecular control of patterning across this axis has important functional implications. Radial axis patterning begins before the cells become postmitotic and is likely linked to the onset of asymmetric expression of secreted factors adjacent to the sensory primordium. This study explores one such asymmetrically expressed gene, Wnt9a, which becomes restricted to the neural edge of the avian auditory organ, the basilar papilla, by embryonic day 5 (E5). Radial patterning is disrupted when Wnt9a is overexpressed throughout the prosensory domain beginning on E3. Sexes were pooled for analysis and sex differences were not studied. Analysis of gene expression and afferent innervation on E6 suggests that ectopic Wnt9a expands the neural-side fate, possibly by re-specifying the abneural fate. RNA sequencing reveals quantitative changes, not only in Wnt-pathway genes, but also in genes involved in axon guidance and cytoskeletal remodeling. By E18, these early patterning effects are manifest as profound changes in cell fates [short hair cells (HCs) are missing], ribbon synapse numbers, outward ionic currents, and efferent innervation. These observations suggest that Wnt9a may be one of the molecules responsible for breaking symmetry across the radial axis of the avian auditory organ. Indirectly, Wnt9a can regulate the mature phenotype whereby afferent axons predominantly innervate neural-side tall HCs, resulting in more ribbon synapses per HC compared with abneural-side short HCs with few ribbons and large efferent synapses.

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“…In addition, epithelial-derived FGF8 and FGF20, expressed in the presumptive epithelial domain of the organ of Corti, function in the specification of distinct cell types, in particular pillar cells, one of the supporting cells found in the developing auditory organ [24,25,26]. Similar to the mouse, in the chick, Fgf3 and Fgf10 function in normal development of the semicircular canals [22,27], whereas Fgfs 2, 8, 10 and 19 influence different aspects of vestibulo-cochlear neuronal development [28,16].…”

Section: Editorialmentioning

confidence: 99%

Inductive and Morphogenetic Responses of the Inner Ear to FGF Signaling

Frenz¹,

Maconochie²

2015

Anat Physiol

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EditorialInner ear development entails a series of sequential inductive tissue interactions where one tissue signals to direct the development of adjacent tissue [s]. Inductive signals from mesodermal, endodermal, and neuroectodermal origin control multiple aspects of early inner ear formation. Signals arising from the endoderm and mesoderm that underlie the presumptive otic field in the cephalic surface ectoderm control induction of the otic placode from this region [1,2], whereas signals emanating from the neuroepithelium of the hindbrain direct invagination of the otic placode to form the otic vesicle. Subsequent morphogenesis of the otic vesicle into the elaborate three-dimensional inner ear occurs in response to yet another set of inductive interactions, this time between the epithelium of the otic vesicle, from which the cochlear and vestibular anlagen form, and the surrounding periotic mesenchyme. Thus all tissue layers in and around the otic region are involved in early inner ear development, and the likely molecular signals leading to these interactions are discussed below.Several members of the fibroblast growth factor (FGF) family from various tissue sources act together to direct different stages of otic vesicle formation [3]. The expression pattern of Fgf3 in the hindbrain adjacent to the developing otic placode [4] originally implicated Fgf3 as a likely candidate in otic induction. Overexpression of Fgf3 in the hindbrain of chicken embryos at a timepoint coincident with invagination of the otic placode resulted in ectopic formation of otic vesicles [2], whereas siRNA blockade of Fgf3 at this developmental stage led to partially invaginated placodes or failure to close the otic pits [2]. Thus in the chicken, Fgf3 is both sufficient and necessary for invagination of the otic placode to form the otic vesicle.However rather than there being any particular "master regulator" of early inner ear development, it has become clear that several FGFs are redundantly required to direct proper formation of the inner ear. Expression patterns of Fgf3 and other FGF ligands (or Fgf genes) partially overlap during inner ear formation, underscoring the importance of defining compensatory relationships between FGFs during this process. Besides FGF3, detection of Fgf10 expression in the hindbrain neuroepithelium coincides both temporally and spatially with development of the otic placode and vesicle [3], supporting its function as an inductive hindbrain-derived signal. Overexpression of Fgf10 in the anterior hindbrain of the mouse leads to the formation of ectopic vesicles that express markers confirming an early otic character, although the complete repertoire of otic marker expression was not obtained [3]. Overexpression of Fgf3 shows a more limited capacity to act as a hindbrain-derived inductive signal. Interestingly, mice homozygous for null mutation of either the Fgf3 [5] or Fgf10 [6] genes revealed unaltered induction of the otic vesicle, and development of seemingly normal albeit smaller otic vesicles. However, ...

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Members of the BMP, Shh, and FGF morphogen families promote chicken statoacoustic ganglion neurite outgrowth and neuron survival in vitro

Cited by 29 publications

References 70 publications

Induction of Neuritogenesis in PC12 Cells by a Pulsed Electromagnetic Field via MEK-ERK1/2 Signaling

Induction of Neuritogenesis in PC12 Cells by a Pulsed Electromagnetic Field via MEK-ERK1/2 Signaling

Wnt9a Can Influence Cell Fates and Neural Connectivity across the Radial Axis of the Developing Cochlea

Inductive and Morphogenetic Responses of the Inner Ear to FGF Signaling

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