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Article: Alteration of Apoptosis in Cleft Palate Formation and Ectomesenchymal Stem Cells Influenced by Retinoic Acid

TitleAlteration of Apoptosis in Cleft Palate Formation and Ectomesenchymal Stem Cells Influenced by Retinoic Acid
Authors
Issue Date2001
Citation
Okajimas Folia Anatomica Japonica, 2001, v. 78 n. 5, p. 179-186 How to Cite?
AbstractIt has been shown that apoptosis is involved in normal embryonic development. The aim of the present study was to elucidate the role and alteration of apoptosis in the pathogenesis of cleft palate induced by retinoic acid (RA) and the ectomesenchymal stem (EMS) cells influenced by RA. RA was administered by gavage to pregnant C57BL/6N strain mice in the experimental group, and the control group received oil alone. Pregnant mice were killed at set periods of time thereafter and histologically analyzed. EMS cells explanted from the palatal shelves of embryonic mice were cultured and characterized by immunohistochemistry, growth curves and population-doubling time. The alterations of apoptosis of EMS cells and developing palatal shelves influenced by RA were evaluated by the terminal deoxynucleotidyl transferase-mediated UTP-biotin nick end-labeling (TUNEL) method. RA-treated mice showed formation of cleft palates resulted from the small size of the palatal shelves and their failure to lift. TUNEL staining showed that the number of apoptotic mesenchymal cells in palatal shelves in the RA-treated mice was increased significantly when compared with the control group. The primary culture of EMS cells proceeded successfully. The population-doubling time of RA-treated cells was much longer compared with non-treated EMS cells. RA also dramatically increased the number of apoptotic cells in EMS cells in vitro. We concluded that EMS cells are the crucial cells in palate development. RA could inhibit the proliferation and induced the apoptosis of EMS cells. The inhibition of growth and excess apoptosis of EMS cells may contribute to the formation of cleft palate and other orofacial congenital malformations.
Persistent Identifierhttp://hdl.handle.net/10722/149603
ISSN
2015 SCImago Journal Rankings: 0.223
References

 

DC FieldValueLanguage
dc.contributor.authorSuwa, Fen_US
dc.contributor.authorJin, Yen_US
dc.contributor.authorLu, Hen_US
dc.contributor.authorXin, LIen_US
dc.contributor.authorTipoe, GLen_US
dc.contributor.authorLau, TYHen_US
dc.contributor.authorTamada, Yen_US
dc.contributor.authorKuroki, Ken_US
dc.contributor.authorFang, YRen_US
dc.date.accessioned2012-06-26T05:55:49Z-
dc.date.available2012-06-26T05:55:49Z-
dc.date.issued2001en_US
dc.identifier.citationOkajimas Folia Anatomica Japonica, 2001, v. 78 n. 5, p. 179-186en_US
dc.identifier.issn0030-154Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/149603-
dc.description.abstractIt has been shown that apoptosis is involved in normal embryonic development. The aim of the present study was to elucidate the role and alteration of apoptosis in the pathogenesis of cleft palate induced by retinoic acid (RA) and the ectomesenchymal stem (EMS) cells influenced by RA. RA was administered by gavage to pregnant C57BL/6N strain mice in the experimental group, and the control group received oil alone. Pregnant mice were killed at set periods of time thereafter and histologically analyzed. EMS cells explanted from the palatal shelves of embryonic mice were cultured and characterized by immunohistochemistry, growth curves and population-doubling time. The alterations of apoptosis of EMS cells and developing palatal shelves influenced by RA were evaluated by the terminal deoxynucleotidyl transferase-mediated UTP-biotin nick end-labeling (TUNEL) method. RA-treated mice showed formation of cleft palates resulted from the small size of the palatal shelves and their failure to lift. TUNEL staining showed that the number of apoptotic mesenchymal cells in palatal shelves in the RA-treated mice was increased significantly when compared with the control group. The primary culture of EMS cells proceeded successfully. The population-doubling time of RA-treated cells was much longer compared with non-treated EMS cells. RA also dramatically increased the number of apoptotic cells in EMS cells in vitro. We concluded that EMS cells are the crucial cells in palate development. RA could inhibit the proliferation and induced the apoptosis of EMS cells. The inhibition of growth and excess apoptosis of EMS cells may contribute to the formation of cleft palate and other orofacial congenital malformations.en_US
dc.languageengen_US
dc.relation.ispartofOkajimas Folia Anatomica Japonicaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntineoplastic Agents - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCleft Palate - Chemically Induced - Pathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMesoderm - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshPalate - Abnormalitiesen_US
dc.subject.meshPregnancyen_US
dc.subject.meshStem Cells - Pathologyen_US
dc.subject.meshTretinoin - Pharmacologyen_US
dc.titleAlteration of Apoptosis in Cleft Palate Formation and Ectomesenchymal Stem Cells Influenced by Retinoic Aciden_US
dc.typeArticleen_US
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_US
dc.identifier.authorityTipoe, GL=rp00371en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11915360-
dc.identifier.scopuseid_2-s2.0-0035753382en_US
dc.identifier.hkuros74721-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035753382&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume78en_US
dc.identifier.issue5en_US
dc.identifier.spage179en_US
dc.identifier.epage186en_US
dc.publisher.placeJapanen_US
dc.identifier.scopusauthoridSuwa, F=6701428537en_US
dc.identifier.scopusauthoridJin, Y=26643271200en_US
dc.identifier.scopusauthoridLu, H=7404843896en_US
dc.identifier.scopusauthoridXin, LI=8159834100en_US
dc.identifier.scopusauthoridTipoe, GL=7003550610en_US
dc.identifier.scopusauthoridLau, TYH=26323763000en_US
dc.identifier.scopusauthoridTamada, Y=7005752601en_US
dc.identifier.scopusauthoridKuroki, K=7102448577en_US
dc.identifier.scopusauthoridFang, YR=7403457335en_US

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