Expression of neurotrophin trk and p75 receptors in quail embryos undergoing gastrulation and neurulation

Zhang, Damin; Yao, Lihua; Bernd, Paulette

doi:10.1002/(sici)1097-0177(199602)205:2<150::aid-aja6>3.0.co;2-h

Cited by 14 publications

(4 citation statements)

References 64 publications

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“…1F). The molecular weight of TrkC in both the outflow tracts and dorsal root ganglia was somewhat higher than expected but similar to previous results from our laboratory (Zhang et al, 1996); this increased molecular weight is probably due to glycosylation. Our immunoblot data reveal only one band, however, suggesting that only the full‐length isoform is present in the developing heart.…”

Section: Resultssupporting

confidence: 91%

Neurotrophin‐3 and TrkC are expressed in the outflow tract of the developing chicken heart

Bernd

Miles

Rozenberg

et al. 2004

Developmental Dynamics

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Section: Resultssupporting

confidence: 91%

Neurotrophin‐3 and TrkC are expressed in the outflow tract of the developing chicken heart

Bernd

Miles

Rozenberg

et al. 2004

Developmental Dynamics

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“…That NT-3 may serve as a mitogen for cardiac myocytes in the looping heart, and during the processes of trabeculation and chamber formation, is supported by evidence of the early localization of this neurotrophin and receptor in the developing heart. Although NT-3 mRNA is detectable in early avian embryos (HH stage 6), when heart precursors reside in the lateral mesodermal plate, no tissue localization has been performed to date (Zhang et al, 1996). Our prior, limited studies in the mouse have documented trk C protein expression by cardiac myocytes at murine embryonic day 9.5, which is similar with regard to cardiac development to avian embryonic day 3 to 4 (Donovan et al, 1996).…”

Section: Figmentioning

confidence: 85%

Trk C Receptor Signaling Regulates Cardiac Myocyte Proliferation during Early Heart Development in Vivo

Lin¹,

Das²,

Schwartz³

et al. 2000

Developmental Biology

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Neurotrophin-3 (NT-3) is a member of the neurotrophin family of growth factors, best characterized by its survival- and differentiation-inducing effects on developing neurons bearing the trk C receptor tyrosine kinase. Through analysis of NT-3 and trk C gene-targeted mice we have identified NT-3 as critically regulating cardiac septation, valvulogenesis, and conotruncal formation. Although these defects could reflect cardiac neural crest dysfunction, the expression of NT-3 and trk C by cardiac myocytes prior to neural crest migration prompted analysis of cell-autonomous actions of NT-3 on cardiac myocytes. Retroviral-mediated overexpression of truncated trk C receptor lacking kinase activity was used to inhibit activation of trk C by endogenous NT-3, during early heart development in ovo. During the first week of chicken development, expression of truncated trk C reduced myocyte clone size by more than 60% of control clones. Direct mitogenic actions of NT-3 on embryonic cardiac myocytes were demonstrated by analysis of BrdU incorporation or PCNA immunoreactivity in control and truncated trk C-expressing clones. Inhibition of trk C signaling reduced cardiac myocyte proliferation during the first week of development, but had no effect at later times. These studies demonstrate that endogenous NT-3:trk C signaling regulates cardiac myocyte proliferation during cardiac looping and the establishment of ventricular trabeculation but that myocyte proliferation becomes NT-3 independent during the second week of embryogenesis.

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“…For example, glial cell line-derived neurotrophic factor and neurotrophin (NT)-3 are essential not only for nervous system development, but also for the normal morphogenesis of kidney and heart, respectively (Donovan et al, 1996;Moore et al, 1996;Pichel et al, 1996;Sanchez et al, 1996). It is not surprising, therefore, that various neurotrophic factors and their receptors are expressed by non-neuronal tissues during key steps of embryogenesis (Timmusk et al, 1993;Williams et al, 1993;Yao et al, 1994;Hellmich et al, 1996;Nichols et al, 1996;Zhang et al, 1996).…”

mentioning

confidence: 99%

Neurotrophin-3 Involvement in the Regulation of Hair Follicle Morphogenesis

Botchkarev

Botchkareva

Albers

et al. 1998

Journal of Investigative Dermatology

151

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Hair follicle epithelium and nervous system share a common ectodermal origin, and some neurotrophins can modulate keratinocyte proliferation and apoptosis. It is therefore reasonable to ask whether growth factors that control neural development are also involved in the regulation of hair follicle morphogenesis. Focusing on neurotrophin-3 (NT-3) and its high-affinity-receptor [tyrosine kinase C (TrkC)], we show that hair placode keratinocytes express TrkC mRNA and immunoreactivity early during murine hair follicle morphogenesis. In later stages of hair follicle development, TrkC mRNA, TrkC-, and NT-3-immunoreactivity are seen in keratinocytes of the proximal hair bulb as well as in dermal papilla fibroblasts. Compared with the corresponding wild-type animals, early stages of hair follicle morphogenesis are significantly accelerated in newborn NT-3 overexpressing mice, whereas these are retarded in newborn heterozygous NT-3 knockout (+/-) mice. These observations suggest that NT-3 is an important growth modulator during morphogenesis and remodeling of neuroectodermal-mesenchymal interaction systems like the hair follicle.

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Expression of neurotrophin trk and p75 receptors in quail embryos undergoing gastrulation and neurulation

Cited by 14 publications

References 64 publications

Neurotrophin‐3 and TrkC are expressed in the outflow tract of the developing chicken heart

Neurotrophin‐3 and TrkC are expressed in the outflow tract of the developing chicken heart

Trk C Receptor Signaling Regulates Cardiac Myocyte Proliferation during Early Heart Development in Vivo

Neurotrophin-3 Involvement in the Regulation of Hair Follicle Morphogenesis

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