Molar tooth development in caspase-3 deficient mice
Jazyk angličtina Země Španělsko Médium print
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
NS41962
NINDS NIH HHS - United States
PubMed
16586350
DOI
10.1387/ijdb.052117em
PII: 052117em
Knihovny.cz E-zdroje
- MeSH
- apoptóza MeSH
- fibroblastový růstový faktor 4 genetika MeSH
- hybridizace in situ MeSH
- kaspasa 3 MeSH
- kaspasy nedostatek genetika MeSH
- messenger RNA genetika metabolismus MeSH
- moláry cytologie embryologie enzymologie MeSH
- myši knockoutované MeSH
- myši MeSH
- odontogeneze genetika fyziologie MeSH
- proliferace buněk MeSH
- proteiny hedgehog MeSH
- trans-aktivátory genetika MeSH
- vývojová regulace genové exprese MeSH
- zubní sklovina cytologie embryologie enzymologie MeSH
- zubní zárodek cytologie embryologie enzymologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- Casp3 protein, mouse MeSH Prohlížeč
- Fgf4 protein, mouse MeSH Prohlížeč
- fibroblastový růstový faktor 4 MeSH
- kaspasa 3 MeSH
- kaspasy MeSH
- messenger RNA MeSH
- proteiny hedgehog MeSH
- Shh protein, mouse MeSH Prohlížeč
- trans-aktivátory MeSH
Tooth morphogenesis is accompanied by apoptotic events which show restricted temporospatial patterns suggesting multiple roles in odontogenesis. Dental apoptosis seems to be caspase dependent and caspase-3 has been shown to be activated during dental apoptosis.Caspase-3 mutant mice on different genetic backgrounds were used to investigate alterations in dental apoptosis and molar tooth morphogenesis. Mouse embryos at E15.5 were analyzed to reveal any changes in enamel knots, which are transient structures eliminated by apoptosis. In caspase-3(-/-) mice on the B57BL/6 background, disorganization of the epithelium was found in the original primary enamel knot area and confirmed by altered expression of Shh. Despite this early defect in molar tooth development, these mutants showed correct formation of secondary enamel knots as indicated by Fgf-4 expression. Analyses of adult molar teeth did not reveal any major alterations in tooth shape, enamel structure or pattern when compared to heterozygote littermates. In caspase-3(-/-) mice on the 129X1/SvJ background, no defects in tooth development were found except the position of the upper molars which developed more posteriorly in the oral cavity. This is likely, however, to be a secondary defect caused by a physical squashing of the face by the malformed brain. The results suggest that although caspase-3 becomes activated and may be essential for dental apoptosis, it does not seem fundamental for formation of normal mineralised molar teeth.
Citace poskytuje Crossref.org
Exploring caspase functions in mouse models
Making the head: Caspases in life and death
Role of Cell Death in Cellular Processes During Odontogenesis
Apoptotic signaling in mouse odontogenesis