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Article: Ihh and Runx2/Runx3 signaling interact to coordinate early chondrogenesis: a mouse model

TitleIhh and Runx2/Runx3 signaling interact to coordinate early chondrogenesis: a mouse model
Authors
Issue Date2013
Citation
PLoS One, 2013, v. 8 n. 2, p. e55296 How to Cite?
AbstractEndochondral bone formation begins with the development of a cartilage intermediate that is subsequently replaced by calcified bone. The mechanisms occurring during early chondrogenesis that control both mesenchymal cell differentiation into chondrocytes and cell proliferation are not clearly understood in vertebrates. Indian hedgehog (Ihh), one of the hedgehog signaling molecules, is known to control both the hypertrophy of chondrocytes and bone replacement; these processes are particularly important in postnatal endochondral bone formation rather than in early chondrogenesis. In this study, we utilized the maternal transfer of 5E1 to E12.5 in mouse embryos, a process that leads to an attenuation of Ihh activity. As a result, mouse limb bud chondrogenesis was inhibited, and an exogenous recombinant IHH protein enhanced the proliferation and differentiation of mesenchymal cells. Analysis of the genetic relationships in the limb buds suggested a more extensive role for Ihh and Runx genes in early chondrogenesis. The transfer of 5E1 decreased the expression of Runx2 and Runx3, whereas an exogenous recombinant IHH protein increased Runx2 and Runx3 expression. Moreover, a transcription factor Gli1 in hedgehog pathway enhances the direct induction of both Runx2 and Runx3 transcription. These findings suggested that Ihh signaling plays an important role in chondrocyte proliferation and differentiation via interactions with Runx2 and Runx3.
Persistent Identifierhttp://hdl.handle.net/10722/184431
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorKim, EJen_US
dc.contributor.authorCho, SWen_US
dc.contributor.authorShin, JOen_US
dc.contributor.authorLee, MJen_US
dc.contributor.authorKim, KSen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2013-07-15T09:45:35Z-
dc.date.available2013-07-15T09:45:35Z-
dc.date.issued2013en_US
dc.identifier.citationPLoS One, 2013, v. 8 n. 2, p. e55296en_US
dc.identifier.urihttp://hdl.handle.net/10722/184431-
dc.description.abstractEndochondral bone formation begins with the development of a cartilage intermediate that is subsequently replaced by calcified bone. The mechanisms occurring during early chondrogenesis that control both mesenchymal cell differentiation into chondrocytes and cell proliferation are not clearly understood in vertebrates. Indian hedgehog (Ihh), one of the hedgehog signaling molecules, is known to control both the hypertrophy of chondrocytes and bone replacement; these processes are particularly important in postnatal endochondral bone formation rather than in early chondrogenesis. In this study, we utilized the maternal transfer of 5E1 to E12.5 in mouse embryos, a process that leads to an attenuation of Ihh activity. As a result, mouse limb bud chondrogenesis was inhibited, and an exogenous recombinant IHH protein enhanced the proliferation and differentiation of mesenchymal cells. Analysis of the genetic relationships in the limb buds suggested a more extensive role for Ihh and Runx genes in early chondrogenesis. The transfer of 5E1 decreased the expression of Runx2 and Runx3, whereas an exogenous recombinant IHH protein increased Runx2 and Runx3 expression. Moreover, a transcription factor Gli1 in hedgehog pathway enhances the direct induction of both Runx2 and Runx3 transcription. These findings suggested that Ihh signaling plays an important role in chondrocyte proliferation and differentiation via interactions with Runx2 and Runx3.-
dc.languageengen_US
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleIhh and Runx2/Runx3 signaling interact to coordinate early chondrogenesis: a mouse modelen_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@hku.hken_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0055296-
dc.identifier.pmcidPMC3562241-
dc.identifier.hkuros215747en_US
dc.identifier.volume8en_US
dc.identifier.issue2en_US
dc.identifier.spagee55296en_US
dc.identifier.epagee55296en_US

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