Hes1 is required for the development of the superior cervical ganglion of sympathetic trunk and the carotid body

Kameda, Yoko; Saitoh, Takayoshi; Nemoto, Noriko; Katoh, Tokio; Iseki, Sachiko

doi:10.1002/dvdy.23819

Cited by 16 publications

(18 citation statements)

References 37 publications

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“…A treatise by Huber, distinguishing neuronal and neuroendocrine lineage and differentiation, is included in this current special issue (Huber 2014). Sympathetic chain neurons and chromaffin cells such as those of the carotid body both require Hes1 expression for their differentiation, perhaps because both are of neural crest origin (Kameda et al 2012). Nerve growth factor signalling is another important factor required not only for survival but also for the initial differentiation of nociceptor dorsal root ganglionic and sympathetic neurons (Ernsberger 2009).…”

Section: Neural Crest Derivatives Of the Peripheral Nervous Systemmentioning

confidence: 99%

Immunocytochemical markers of neuronal maturation in human diagnostic neuropathology

Sarnat

2014

Cell Tissue Res

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Histological descriptions of morphogenesis in human fetal brain and in malformations and tumours can now be supplemented by the timing and sequence of the maturation of individual neurons. In human neuropathology, this is principally achieved by immunocytochemical reactivities used as maturational markers of neuronal properties denoted by molecules and cell products. Cytological markers can appear early and then regress, often being replaced by more mature molecules, or might not exhibit the onset of immunoreactivity until a certain stage of neuronal differentiation is achieved, some early, others intermediate and some late during the maturational process. Inter-specific differences occur in some structures of the brain. The classification of markers of neuronal maturation can be based, in addition to those mentioned above, on several criteria: cytological localisation, water solubility, biochemical nature of the antigen, specificity and various technical factors. The most useful immunocytochemical markers of neuronal maturation in human neuropathology are NeuN, synaptophysin, calretinin and other calcium-binding molecules, various microtubule-associated proteins and chromogranins. Non-antibody histochemical stains that denote maturational processes include luxol fast blue for myelination, acridine orange fluorochrome for nucleic acids, mitochondrial respiratory chain enzymes and argentophilic impregnations. Neural crest derivatives of the peripheral nervous system, including chromaffin and neuroendocrine cells, have special features that are shared and others that differ greatly between lineages. Other techniques used in human diagnostic neuropathology, particularly as applied to tumours, include chromosomal and genetic analyses, the mTOR signalling pathway, BRAF V600E and other tumour-suppressor gene products, transcription products of developmental genes and the proliferation index of the tumour cells and of mitotic neuroepithelial cells.

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Section: Neural Crest Derivatives Of the Peripheral Nervous Systemmentioning

confidence: 99%

Immunocytochemical markers of neuronal maturation in human diagnostic neuropathology

Sarnat

2014

Cell Tissue Res

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“…Ascl1 has been implicated in development of neuronal markers for both sympathetic and parasympathetic CG neurons, 99 , 101 , 102 Phox2a, and Phox2b, are positive regulators for expression of the noradrenergic synthesizing enzyme dopamine β-hydroxylase (DBH), 103 - 105 Gata3 is vital for tyrosine hydroxylase (TH; rate-limiting enzyme in NE synthesis) expression, 106 - 108 and Hand2 is essential for maintaining the catecholaminergic phenotype in development 109 - 113 and in adults 114 . In addition to broad control exerted by dorsal aorta BMPs over these transcription factors, a degree of cross-regulation exists, including repression of Ascl1 by Hes genes, which are effectors of Notch signaling 115 . In addition, a role for microRNAs in the differentiation of sympathetic NCCs has recently been proposed; deletion of the microRNA-processing gene Dicer in mouse embryos causes severe hypoplastic sympathetic ganglia in E15 but not E11-E13 embryos 116 .…”

Section: Development Of Cardiac Autonomic Innervationmentioning

confidence: 99%

Autonomic cardiac innervation

Hasan

2013

Organogenesis

126

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Autonomic cardiac neurons have a common origin in the neural crest but undergo distinct developmental differentiation as they mature toward their adult phenotype. Progenitor cells respond to repulsive cues during migration, followed by differentiation cues from paracrine sources that promote neurochemistry and differentiation. When autonomic axons start to innervate cardiac tissue, neurotrophic factors from vascular tissue are essential for maintenance of neurons before they reach their targets, upon which target-derived trophic factors take over final maturation, synaptic strength and postnatal survival. Although target-derived neurotrophins have a central role to play in development, alternative sources of neurotrophins may also modulate innervation. Both developing and adult sympathetic neurons express proNGF, and adult parasympathetic cardiac ganglion neurons also synthesize and release NGF. The physiological function of these “non-classical” cardiac sources of neurotrophins remains to be determined, especially in relation to autocrine/paracrine sustenance during development. Cardiac autonomic nerves are closely spatially associated in cardiac plexuses, ganglia and pacemaker regions and so are sensitive to release of neurotransmitter, neuropeptides and trophic factors from adjacent nerves. As such, in many cardiac pathologies, it is an imbalance within the two arms of the autonomic system that is critical for disease progression. Although this crosstalk between sympathetic and parasympathetic nerves has been well established for adult nerves, it is unclear whether a degree of paracrine regulation occurs across the autonomic limbs during development. Aberrant nerve remodeling is a common occurrence in many adult cardiovascular pathologies, and the mechanisms regulating outgrowth or denervation are disparate. However, autonomic neurons display considerable plasticity in this regard with neurotrophins and inflammatory cytokines having a central regulatory function, including in possible neurotransmitter changes. Certainly, neurotrophins and cytokines regulate transcriptional factors in adult autonomic neurons that have vital differentiation roles in development. Particularly for parasympathetic cardiac ganglion neurons, additional examinations of developmental regulatory mechanisms will potentially aid in understanding attenuated parasympathetic function in a number of conditions, including heart failure.

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“…Some neuropoietic cytokines, including ciliary neurotrophic factor (CNTF) and LIF, are able to robustly induce a NA-to-ACh switch in this cell type in culture, and thus these cells have been invoked as a potential model system for understanding the sudomotor sympathetic noradrenergic-cholinergic switch in vivo (reviewed in (Ernsberger and Rohrer 1999)). However, the SCG, in vivo, is a sympathetic ganglion virtually devoid of cholinergic neurons, uses a different set of transcription factors to drive noradrenergic differentiation than the stellate and more caudal ganglia (Kameda et al 2012; Lo et al 1999; Howard 2005), and does not innervate target tissues in common with those of cholinergic sudomotor neurons of the stellate and other sympathetic ganglia (Flett and Bell 1991). …”

Section: Introductionmentioning

confidence: 99%

Satb2-Independent Acquisition of the Cholinergic Sudomotor Phenotype in Rodents

Schütz¹,

Schäfer²,

Gördes³

et al. 2014

Cell Mol Neurobiol

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Expression of Satb2 (Special AT-rich sequence-binding protein-2) elicits expression of the vesicular acetylcholine transporter (VAChT) and choline acetyltransferase (ChAT) in cultured rat sympathetic neurons exposed to soluble differentiation factors. Here, we determined whether or not Satb2 plays a similar role in cholinergic differentiation in vivo, by comparing the postnatal profile of Satb2 expression in the rodent stellate ganglion to that of VAChT and ChAT. Throughout postnatal development, VAChT and ChAT were found to be co-expressed in a numerically stable subpopulation of rat stellate ganglion neurons. Nerve fibers innervating rat forepaw sweat glands on P1 were VAChT immunoreactive, while ChAT was detectable at this target only after P5. The postnatal abundance of VAChT transcripts in the stellate ganglion was at maximum already on P1, whereas ChAT mRNA levels increased from low levels on P1 to reach maximum levels between P5 and P21. Satb2 mRNA was detected in cholinergic neurons in the stellate ganglion beginning with P8, thus coincident with the onset of unequivocal detection of ChAT immunoreactivity in forepaw sweat gland endings. Satb2 knockout mice exhibited no change in the P1 cholinergic VAChT/ChAT co-phenotype in stellate ganglion neurons. Thus, cholinergic phenotype maturation involves first, early target (sweat-gland)-independent expression and trafficking of VAChT, and later, potentially target- and Satb2-dependent elevation of ChAT mRNA and protein transport into sweat gland endings. In rat sudomotor neurons that, unlike mouse sudomotor neurons, co-express calcitonin gene-related peptide (CGRP), Satb2 may also be related to the establishment of species-specific neuropeptide co-phenotypes during postnatal development.

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Hes1 is required for the development of the superior cervical ganglion of sympathetic trunk and the carotid body

Cited by 16 publications

References 37 publications

Immunocytochemical markers of neuronal maturation in human diagnostic neuropathology

Immunocytochemical markers of neuronal maturation in human diagnostic neuropathology

Autonomic cardiac innervation

Satb2-Independent Acquisition of the Cholinergic Sudomotor Phenotype in Rodents

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