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Sonic hedgehog regulates the proliferation, differentiation, and migration of enteric neural crest cells in gut.

Fu M, Lui VC, Sham MH, Pachnis V, Tam PK - J. Cell Biol. (2004)

Bottom Line: The pro-neurogenic effect of glial cell line--derived neurotrophic factor (GDNF) on NCCs was abolished by Shh.In gut explants, NCCs migrated from the explants onto the adjacent substratum if GDNF was added, whereas addition of Shh abolished this migration.Our data suggest that Shh controls the proliferation and differentiation of NCCs and modulates the responsiveness of NCCs toward GDNF inductions.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, The University of Hong Kong, 21 Sassoon Rd., Pokfulam, Hong Kong, HKSAR China.

ABSTRACT
Enteric neural crest cells (NCCs) migrate and colonize the entire gut and proliferate and differentiate into neurons and glia of the enteric nervous system in vertebrate embryos. We have investigated the mitogenic and morphogenic functions of Sonic hedgehog (Shh) on enteric NCCs in cell and organ culture. Enteric NCCs expressed Shh receptor Patched and transcripts encoding the Shh signal transducer (Gli1). Shh promoted the proliferation and inhibited the differentiation of NCCs. The pro-neurogenic effect of glial cell line--derived neurotrophic factor (GDNF) on NCCs was abolished by Shh. In gut explants, NCCs migrated from the explants onto the adjacent substratum if GDNF was added, whereas addition of Shh abolished this migration. Neuronal differentiation and coalescence of neural crest--derived cells into myenteric plexuses in explants was repressed by the addition of Shh. Our data suggest that Shh controls the proliferation and differentiation of NCCs and modulates the responsiveness of NCCs toward GDNF inductions.

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Shh regulates multiple aspects of growth of NCCs in the gut. Shh, GDNF, and EDN3 act together to orchestrate the development and the concentric organization of NCCs and musculature of the developing gut. Shh promotes the proliferation and inhibits the differentiation of NCCs. Shh suppresses the pro-neurogenic effects of GDNF on NCCs. Shh and EDN3 restricts the GDNF-induced NCC migration. Shh induces muscle differentiation of mesenchyme, which in turn affects the neural plexus formation.
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fig9: Shh regulates multiple aspects of growth of NCCs in the gut. Shh, GDNF, and EDN3 act together to orchestrate the development and the concentric organization of NCCs and musculature of the developing gut. Shh promotes the proliferation and inhibits the differentiation of NCCs. Shh suppresses the pro-neurogenic effects of GDNF on NCCs. Shh and EDN3 restricts the GDNF-induced NCC migration. Shh induces muscle differentiation of mesenchyme, which in turn affects the neural plexus formation.

Mentions: In conclusion, gut endoderm-derived Shh and mesenchyme-derived factors act together to orchestrate the development and the concentric organization of NCCs and musculature of developing gut (Fig. 9). Furthermore, our data show that NCCs can be maintained in culture without losing stem cell properties in the presence of Shh. The practicality of using Shh in the isolation of NCCs for cell replacement therapy for the treatment of NCC-associated anomalies deserves further investigation.


Sonic hedgehog regulates the proliferation, differentiation, and migration of enteric neural crest cells in gut.

Fu M, Lui VC, Sham MH, Pachnis V, Tam PK - J. Cell Biol. (2004)

Shh regulates multiple aspects of growth of NCCs in the gut. Shh, GDNF, and EDN3 act together to orchestrate the development and the concentric organization of NCCs and musculature of the developing gut. Shh promotes the proliferation and inhibits the differentiation of NCCs. Shh suppresses the pro-neurogenic effects of GDNF on NCCs. Shh and EDN3 restricts the GDNF-induced NCC migration. Shh induces muscle differentiation of mesenchyme, which in turn affects the neural plexus formation.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2172437&req=5

fig9: Shh regulates multiple aspects of growth of NCCs in the gut. Shh, GDNF, and EDN3 act together to orchestrate the development and the concentric organization of NCCs and musculature of the developing gut. Shh promotes the proliferation and inhibits the differentiation of NCCs. Shh suppresses the pro-neurogenic effects of GDNF on NCCs. Shh and EDN3 restricts the GDNF-induced NCC migration. Shh induces muscle differentiation of mesenchyme, which in turn affects the neural plexus formation.
Mentions: In conclusion, gut endoderm-derived Shh and mesenchyme-derived factors act together to orchestrate the development and the concentric organization of NCCs and musculature of developing gut (Fig. 9). Furthermore, our data show that NCCs can be maintained in culture without losing stem cell properties in the presence of Shh. The practicality of using Shh in the isolation of NCCs for cell replacement therapy for the treatment of NCC-associated anomalies deserves further investigation.

Bottom Line: The pro-neurogenic effect of glial cell line--derived neurotrophic factor (GDNF) on NCCs was abolished by Shh.In gut explants, NCCs migrated from the explants onto the adjacent substratum if GDNF was added, whereas addition of Shh abolished this migration.Our data suggest that Shh controls the proliferation and differentiation of NCCs and modulates the responsiveness of NCCs toward GDNF inductions.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, The University of Hong Kong, 21 Sassoon Rd., Pokfulam, Hong Kong, HKSAR China.

ABSTRACT
Enteric neural crest cells (NCCs) migrate and colonize the entire gut and proliferate and differentiate into neurons and glia of the enteric nervous system in vertebrate embryos. We have investigated the mitogenic and morphogenic functions of Sonic hedgehog (Shh) on enteric NCCs in cell and organ culture. Enteric NCCs expressed Shh receptor Patched and transcripts encoding the Shh signal transducer (Gli1). Shh promoted the proliferation and inhibited the differentiation of NCCs. The pro-neurogenic effect of glial cell line--derived neurotrophic factor (GDNF) on NCCs was abolished by Shh. In gut explants, NCCs migrated from the explants onto the adjacent substratum if GDNF was added, whereas addition of Shh abolished this migration. Neuronal differentiation and coalescence of neural crest--derived cells into myenteric plexuses in explants was repressed by the addition of Shh. Our data suggest that Shh controls the proliferation and differentiation of NCCs and modulates the responsiveness of NCCs toward GDNF inductions.

Show MeSH
Related in: MedlinePlus