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Article: Retinoic acid modulates chondrogenesis in the developing mouse cranial base

TitleRetinoic acid modulates chondrogenesis in the developing mouse cranial base
Authors
Issue Date2011
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/
Citation
Journal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2011, v. 316 B n. 8, p. 574-583 How to Cite?
AbstractThe retinoic acid (RA) signaling pathway is known to play important roles during craniofacial development and skeletogenesis. However, the specific mechanism involving RA in cranial base development has not yet been clearly described. This study investigated how RA modulates endochondral bone development of the cranial base by monitoring the RA receptor RARγ, BMP4, and markers of proliferation, programmed cell death, chondrogenesis, and osteogenesis. We first examined the dynamic morphological and molecular changes in the sphenooccipital synchondrosis-forming region in the mouse embryo cranial bases at E12-E16. In vitro organ cultures employing beads soaked in RA and retinoid-signaling inhibitor citral were compared. In the RA study, the sphenooccipital synchondrosis showed reduced cartilage matrix and lower BMP4 expression while hypertrophic chondrocytes were replaced with proliferating chondrocytes. Retardation of chondrocyte hypertrophy was exhibited in citral-treated specimens, while BMP4 expression was slightly increased and programmed cell death was induced within the sphenooccipital synchondrosis. Our results demonstrate that RA modulates chondrocytes to proliferate, differentiate, or undergo programmed cell death during endochondral bone formation in the developing cranial base. © 2011 Wiley Periodicals, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/169587
ISSN
2015 Impact Factor: 2.083
2015 SCImago Journal Rankings: 1.333
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwon, HJen_US
dc.contributor.authorShin, JOen_US
dc.contributor.authorLee, JMen_US
dc.contributor.authorCho, KWen_US
dc.contributor.authorLee, MJen_US
dc.contributor.authorCho, SWen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2012-10-25T04:53:11Z-
dc.date.available2012-10-25T04:53:11Z-
dc.date.issued2011en_US
dc.identifier.citationJournal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2011, v. 316 B n. 8, p. 574-583en_US
dc.identifier.issn1552-5007en_US
dc.identifier.urihttp://hdl.handle.net/10722/169587-
dc.description.abstractThe retinoic acid (RA) signaling pathway is known to play important roles during craniofacial development and skeletogenesis. However, the specific mechanism involving RA in cranial base development has not yet been clearly described. This study investigated how RA modulates endochondral bone development of the cranial base by monitoring the RA receptor RARγ, BMP4, and markers of proliferation, programmed cell death, chondrogenesis, and osteogenesis. We first examined the dynamic morphological and molecular changes in the sphenooccipital synchondrosis-forming region in the mouse embryo cranial bases at E12-E16. In vitro organ cultures employing beads soaked in RA and retinoid-signaling inhibitor citral were compared. In the RA study, the sphenooccipital synchondrosis showed reduced cartilage matrix and lower BMP4 expression while hypertrophic chondrocytes were replaced with proliferating chondrocytes. Retardation of chondrocyte hypertrophy was exhibited in citral-treated specimens, while BMP4 expression was slightly increased and programmed cell death was induced within the sphenooccipital synchondrosis. Our results demonstrate that RA modulates chondrocytes to proliferate, differentiate, or undergo programmed cell death during endochondral bone formation in the developing cranial base. © 2011 Wiley Periodicals, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/en_US
dc.relation.ispartofJournal of Experimental Zoology Part B: Molecular and Developmental Evolutionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effects - Physiologyen_US
dc.subject.meshBone Morphogenetic Protein 4 - Drug Effects - Metabolismen_US
dc.subject.meshCell Differentiation - Drug Effects - Physiologyen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshChondrocytes - Cytology - Drug Effectsen_US
dc.subject.meshChondrogenesis - Drug Effects - Physiologyen_US
dc.subject.meshIntegrin-Binding Sialoprotein - Drug Effects - Metabolismen_US
dc.subject.meshKi-67 Antigen - Drug Effects - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMonoterpenes - Pharmacologyen_US
dc.subject.meshOrgan Culture Techniquesen_US
dc.subject.meshOsteogenesis - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Retinoic Acid - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshSkull Base - Cytology - Drug Effects - Embryology - Metabolismen_US
dc.subject.meshTretinoin - Metabolism - Pharmacologyen_US
dc.titleRetinoic acid modulates chondrogenesis in the developing mouse cranial baseen_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jez.b.21432en_US
dc.identifier.pmid21826789-
dc.identifier.scopuseid_2-s2.0-81355149686en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-81355149686&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume316 Ben_US
dc.identifier.issue8en_US
dc.identifier.spage574en_US
dc.identifier.epage583en_US
dc.identifier.isiWOS:000297576000003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKwon, HJ=18836582500en_US
dc.identifier.scopusauthoridShin, JO=37361704500en_US
dc.identifier.scopusauthoridLee, JM=38862129700en_US
dc.identifier.scopusauthoridCho, KW=7403956665en_US
dc.identifier.scopusauthoridLee, MJ=36054770900en_US
dc.identifier.scopusauthoridCho, SW=32967447200en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US

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