Neural Crest-Derived Cells Isolated from the Gut by Immunoselection DeveLop Neuronal and Glial Phenotypes When Cultured on Laminin

Pomeranz, Howard D.; Rothman, Taube P.; Chalazonitis, Alcmène; Tennyson, Virginia M.; Gershon, Michael D.

doi:10.1006/dbio.1993.1082

Cited by 67 publications

(39 citation statements)

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“…Gershon and colleagues (37) have proposed that an excess of laminin expression in the developing Is hindgut may promote premature differentiation of the neuroblast prior to completion of migration. Endothelins can influence the production of extracellular matrix components (38).…”

Section: Resultsmentioning

confidence: 99%

Null mutation of endothelin receptor type B gene in spotting lethal rats causes aganglionic megacolon and white coat color.

Gariepy

Cass

Yanagisawa³

1996

Proc. Natl. Acad. Sci. U.S.A.

198

154

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Mutations in the gene encoding the endothelin receptor type B (EDNRB) produce congenital aganglionic megacolon and pigment abnormalities in mice and humans. Here we report a naturally occurring null mutation of the EDNRB gene in spotting lethal (si) rats, which exhibit aganglionic megacolon associated with white coat color. We found a 301-bp deletion spanning the exon 1-intron 1 junction of the EDNRB gene in sl rats. A restriction fragment length polymorphism caused by this deletion perfectly cosegregates with the sl phenotype. The deletion leads to production of an aberrantly spliced EDNRB mRNA that lacks the coding sequence for the first and second putative transmembrane domains of the G-protein-coupled receptor. Radioligand binding assays revealed undetectable levels of functional EDNRB in tissues from homozygous sl/sl rats. We conclude that EDNRB plays an essential role in the normal development of two neural crest-derived cell lineages, epidermal melanocytes and enteric neurons, in three mammalian species-humans, mice, and rats. The EDNRB-deficient rat may also prove valuable in defining the postnatal physiologic role of this receptor.

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Section: Resultsmentioning

confidence: 99%

Null mutation of endothelin receptor type B gene in spotting lethal rats causes aganglionic megacolon and white coat color.

Gariepy

Cass

Yanagisawa³

1996

Proc. Natl. Acad. Sci. U.S.A.

198

154

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“…disease suggest that an abnormal microenvironment in the distal developing intestine provides an unfavorable substrate for vagal crest colonization (47)(48)(49)(50)(51)(52)(53)(54). There is evidence that the absence of EDNRB activation by EDN3 leads to increased expression of laminin that may result in premature differentiation of neural crest-derived cells and contribute to their incomplete colonization of the gut (55,56). Aggregation chimera studies in mice suggest that activation of the EDNRB receptor on the colonizing neuroblasts leads to local environmental or extracellular signals, which promote colonization.…”

Section: Discussionmentioning

confidence: 99%

Transgenic expression of the endothelin-B receptor prevents congenital intestinal aganglionosis in a rat model of Hirschsprung disease.

Gariepy¹,

Williams²,

Richardson³

et al. 1998

J. Clin. Invest.

164

145

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The spotting lethal rat, a naturally occurring rodent model of Hirschsprung disease, carries a deletion in the endothelin-B receptor ( EDNRB ) gene that abrogates expression of functional EDNRB receptors. Rats homozygous for this mutation ( sl ) exhibit coat color spotting and congenital intestinal aganglionosis. These deficits result from failure of the neural crest-derived epidermal melanoblasts and enteric nervous system (ENS) precursors to completely colonize the skin and intestine, respectively. We demonstrate that during normal rat development, the EDNRB mRNA expression pattern is consistent with expression by ENS precursors throughout gut colonization. We used the human dopamine-␤ -hydroxylase ( D ␤ H ) promoter to direct transgenic expression of EDNRB to colonizing ENS precursors in the sl/sl rat. The D ␤ H-EDNRB transgene compensates for deficient endogenous EDNRB in these rats and prevents the intestinal defect. The transgene has no effect on coat color spotting, indicating the critical time for EDNRB expression in enteric nervous system development begins after separation of the melanocyte lineage from the ENS lineage and their common precursor. The transgene dosage affects both the incidence and severity of the congenital intestinal defect, suggesting dosage-dependent events downstream of EDNRB activation in ENS development.

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“…Crest-and noncrest-derived cells were isolated from dissociated fetal bowel by a process of positive and negative immunoselection with antibodies to human natural killer cell antigen HN K-1 (Erickson et al, 1989;Pomeranz et al, 1993;Chalazonitis et al, 1994) or p75 N TR (Baetge et al, 1990a;Chalazonitis et al, 1997Chalazonitis et al, , 1998a as described previously. HN K-1 antibodies were derived from cells purchased from American T ype Culture Collection (Rockville, MD).…”

Section: Methodsmentioning

confidence: 99%

Neurotrophin-3 Is Required for the Survival–Differentiation of Subsets of Developing Enteric Neurons

et al. 2001

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Neurotrophin-3 (NT-3) promotes enteric neuronal development in vitro; nevertheless, an enteric nervous system (ENS) is present in mice lacking NT-3 or TrkC. We thus analyzed the physiological significance of NT-3 in ENS development. Subsets of neurons developing in vitro in response to NT-3 became NT-3 dependent; NT-3 withdrawal led to apoptosis, selectively in TrkC-expressing neurons. Antibodies to NT-3, which blocked the developmental response of enteric crest-derived cells to exogenous NT-3, did not inhibit neuronal development in cultures of isolated crest-derived cells but did so in mixed cultures of crest-and non-neural crest-derived cells; therefore, the endogenous NT-3 that supports enteric neuronal development is probably obtained from noncrest-derived mesenchymal cells. In mature animals, retrograde transport of 125 I-NT-3, injected into the mucosa, labeled neurons in ganglia of the submucosal but not myenteric plexus; injections of 125 I-NT-3 into myenteric ganglia, the tertiary plexus, and muscle, labeled neurons in underlying submucosal and distant myenteric ganglia. The labeling pattern suggests that NT-3-dependent submucosal neurons may be intrinsic primary afferent and/or secretomotor, whereas NT-3-dependent myenteric neurons innervate other myenteric ganglia and/or the longitudinal muscle. Myenteric neurons were increased in number and size in transgenic mice that overexpress NT-3 directed to myenteric ganglia by the promoter for dopamine ␤-hydroxylase. The numbers of neurons were regionally reduced in both plexuses in mice lacking NT-3 or TrkC. A neuropoietic cytokine (CNTF) interacted with NT-3 in vitro, and if applied sequentially, compensated for NT-3 withdrawal. These observations indicate that NT-3 is required for the normal development of the ENS.

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Neural Crest-Derived Cells Isolated from the Gut by Immunoselection DeveLop Neuronal and Glial Phenotypes When Cultured on Laminin

Cited by 67 publications

References 0 publications

Null mutation of endothelin receptor type B gene in spotting lethal rats causes aganglionic megacolon and white coat color.

Null mutation of endothelin receptor type B gene in spotting lethal rats causes aganglionic megacolon and white coat color.

Transgenic expression of the endothelin-B receptor prevents congenital intestinal aganglionosis in a rat model of Hirschsprung disease.

Neurotrophin-3 Is Required for the Survival–Differentiation of Subsets of Developing Enteric Neurons

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