Signals and Switches in Mammalian Neural Crest Cell Differentiation

Bhatt, Shachi; Díaz, Raúl E.; Trainor, Paul A.

doi:10.1101/cshperspect.a008326

Cited by 183 publications

(165 citation statements)

References 208 publications

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“…We therefore hypothesized that SHH signaling-associated cleft lip occurred via disruption of WNT-mediated p63/IRF6 signaling. Via in situ hybridization, we found p63/ IRF6 signaling noticeably inhibited at the lambdoidal junction in cells (CNCs) play critical roles in producing cartilage, bone, and connective tissues as well as regulating facial patterning (26)(27)(28). SHH signaling has been shown to be a critical regulator of CNC development (29).…”

mentioning

confidence: 99%

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

Kurosaka¹,

Iulianella²,

Williams³

et al. 2014

J. Clin. Invest.

103

128

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Cleft lip, which results from impaired facial process growth and fusion, is one of the most common cranio facial birth defects. Many genes are known to be involved in the etiology of this disorder; however, our under standing of cleft lip pathogenesis remains incomplete. In the present study, we uncovered a role for sonic hedgehog (SHH) signaling during lip fusion. Mice carrying compound mutations in hedgehog acyltransferase (Hhat) and patched1 (Ptch1) exhibited perturbations in the SHH gradient during frontonasal development, which led to hypoplastic nasal process outgrowth, epithelial seam persistence, and cleft lip. Further investi gation revealed that enhanced SHH signaling restricts canonical WNT signaling in the lambdoidal region by promoting expression of genes encoding WNT inhibitors. Moreover, reduction of canonical WNT signaling perturbed p63/interferon regulatory factor 6 (p63/IRF6) signaling, resulting in increased proliferation and decreased cell death, which was followed by persistence of the epithelial seam and cleft lip. Consistent with our results, mutations in genes that disrupt SHH and WNT signaling have been identified in both mice and humans with cleft lip. Collectively, our data illustrate that altered SHH signaling contributes to the etiology and pathogenesis of cleft lip through antagonistic interactions with other gene regulatory networks, including the canonical WNT and p63/IRF6 signaling pathways.

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mentioning

confidence: 99%

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

Kurosaka¹,

Iulianella²,

Williams³

et al. 2014

J. Clin. Invest.

103

128

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“…Utóbbiakról viszont nem tudjuk, hogy azonosak-e a dorsolateralis úton migráló NC-sejtekből fejlődő és a szervezetben található pigmentsejtek döntő többségét kitevő melanocytákkal (l. még később!) [4,12].…”

Section: áBraunclassified

A pluri- és multipotencia határán: a ganglionléc őssejtjei

et al. 2015

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A ganglionléc a gerinces embriókban megjelenő átmeneti, multipotens, vándorló sejtpopuláció, amiből a perifériás idegrendszer idegi és gliális elemeitől kezdve a craniofacialis terület ectomesenchymalis származékain vagy a bőr pigmentsejtjein át számos struktúra származtatható. Érdekes módon a ganglionléc-eredetű őssejtek nem csak az embrionális ganglionlécben vannak jelen, hanem megtalálhatók az általuk betelepített embrionális és felnőttkori szövetek-ben is. Ezek a posztmigrációs őssejtek -legalábbis részlegesen -tükrözik elődeik multipotenciáját. Ráadásul az olyan ganglionléc-eredetű, terminálisan differenciálódott sejtek, mint például a Schwann-sejtek és a melanocyták, bármikor képesek őssejtszerű progenitorokká dedifferenciálódni. Az összefoglaló tanulmányban a szerzők bemutatják, hogy mit tudunk jelenleg ezekről a különleges plaszticitású őssejtekről és milyen potenciális alkalmazási lehetőségek merül-nek fel velük kapcsolatban a regeneratív orvoslás területén. Orv. Hetil., 2015, 156(42), 1683-1694. Kulcsszavak: ectomesenchyma, ganglionléc, őssejtek, plaszticitás At the border of pluri-and multipotency: the neural crest stem cellsThe neural crest is a transient, multipotent, migratory cell population that is unique to vertebrate embryos and gives rise to many derivatives, ranging from the neuronal and glial components of the peripheral nervous system to the ectomesenchymal derivatives of the craniofacial area and pigment cells in the skin. Intriguingly, the neural crest derived stem cells are not only present in the embryonic neural crest, but also in their target tissues in the fetus and adult. These postmigratory stem cells, at least partially, resemble their multipotency. Moreover, fully differentiated neural crest-derived cells such as Schwann cells and melanocytes are able to dedifferentiate into stem-like progenitors.Here the authors review current understanding of this unique plasticity and its potential application in stem cell biology as well as in regenerative medicine. ÖSSZEFOGLALÓ KÖZLEMÉNYRövidítések BMP = csont morfogenetikus fehérje; CFP = kék színű fl uoreszcens fehérje; CIL = sejtek mozgásának kontakt gátlása; DRG = dorsalis gyökérdúcok; EGF = epidermalis növekedési faktor; EMT = epithelialis-mesenchymalis tranzíció; Eph = ephrinreceptor; ER = ösztrogénreceptor; FGF = fi broblastnö-vekedési faktor; GDNF = gliaeredetű növekedési faktor; GFAP = gliális fi brilláris savanyú fehérje; GFP = zöld fl uoreszcens fehérje; IL = interleukin; LIF = leukaemiagátló faktor; MCP-1 = monocyta kemotaktikus fehérje-1; MSC = mesenchymalis őssejt; NC = ganglionléc; NCSC = ganglionlécőssejt; NGF = idegi eredetű növekedési faktor; PDGF = vérlemezke-eredetű növekedési faktor; R26R = Rosa26 riporter gén(komplex)

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“…Neural crest cells forming sympathetic ganglia also migrate both cranially and caudally and extend these trunks into cervical and pelvic regions. The migration and localization of neural crest cells are controlled by bone morphogenetic proteins (BMP) secreted by dorsal aorta [7][8][9].…”

Section: The Autonomic Nervous Systemmentioning

confidence: 99%

Anatomic Origin and Molecular Genetics in Neuroblastoma

Tosun¹,

Karabekir²,

Durmaz³

et al. 2017

Neuroblastoma - Current State and Recent Updates

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Neuroblastoma is considered as the most common extracranial solid tumor occurring during childhood, but takes place rarely after the age of 10 years. The tumors are considered as embryonal tumors that result from the fetal or early postnatal life development and are formed from neural crest-derived cells, and their origination is from the early nerve cells which are called as neuroblasts of sympathetic nervous system. Being heterogeneous in their biological, genetic, and morphological characteristics, tumors which are distinct from other solid tumors due to their biological heterogeneity result in the clinical pattern changes from spontaneous regression to a highly aggressive metastatic disease. Neuroblastoma tumorigenesis is regulated by Myc oncogene, leading to aggressive tumor subset. Many epigenetic factors play crucial role in the disease induction and development, while regulatory effect and outcome result in epigenetic patterns distinguishing neuroectoderm, neural crest, and more mature neural states. Neuroblastoma patients' clinical management is based on prognostic categories subtracted from studies correlating outcome and clinico-biological variables. Neuroblastoma anatomic boundaries include primarily autonomic nervous system besides other rare locations. Neuroblastoma molecular pathogenesis classifies the tumor according to the different clinical behaviors that are important for the improvement of the patients outcome and overall survival according to the different therapy modalities applied.

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Signals and Switches in Mammalian Neural Crest Cell Differentiation

Cited by 183 publications

References 208 publications

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

A pluri- és multipotencia határán: a ganglionléc őssejtjei

Anatomic Origin and Molecular Genetics in Neuroblastoma

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