Dlx5 Is a Positive Regulator of Chondrocyte Differentiation during Endochondral Ossification

Developmental Biology

Robert A. Kosher¹  Deborah Ferrari¹ 

[1] Department of BioStructure and Function, University of Connecticut Health Center, Farmington, CT, 06030

关键词: Dlx5;    chondrocyte differentiation;    chondrocyte maturation;    chondrocyte hypertrophy;    endochondral ossification;    osteoblast differentiation;    bone development;    limb;   

DOI  :  10.1006/dbio.2002.0862

学科分类：生物科学（综合）

来源: Academic Press

【 摘 要 】

Theprocessofendochondralossificationinwhichthebonesofthelimbareformedaftergenerationofcartilagemodelsisdependentonapreciselyregulatedprogramofchondrocytematuration.Here,weshowthatthehomeobox-containinggeneDlx5isexpressedattheonsetofchondrocytematurationduringtheconversionofimmatureproliferatingchondrocytesintopostmitotichypertrophyingchondrocytes,acriticalstepinthematurationprocess.Moreover,retroviralmisexpressionofDlx5duringdifferentiationoftheskeletalelementsofthechicklimbinvivoresultsintheformationofseverelyshortenedskeletalelementsthatcontainexcessivenumbersofhypertrophyingchondrocyteswhichextendintoectopicregions,includingsitesnormallyoccupiedbyimmaturechondrocytes.Theexpansionintheextentofhypertrophicmaturationdetectablehistologicallyisaccompaniedbyexpandedandupregulateddomainsofexpressionofmolecularmarkersofchondrocytematuration,particularlytypeXcollagenandosteopontin,andbyexpansionofmineralizedcartilagematrix,whichischaracteristicofterminalhypertrophicdifferentiation.Furthermore,Dlx5misexpressionmarkedlyreduceschondrocyteproliferationconcomitantwithpromotinghypertrophicmaturation.Takentogether,theseresultsindicatethatDlx5isapositiveregulatorofchondrocytematurationandsuggestthatitregulatestheprocessatleastinpartbypromotingconversionofimmatureproliferatingchondrocytesintohypertrophyingchondrocytes.RetroviralmisexpressionofDlx5alsoenhancesformationofperiostealbone,whichisderivedfromtheDlx5-expressingperichondriumthatsurroundsthediaphysesofthecartilagemodels.ThissuggeststhatDlx5maybeinvolvedinregulatingosteoblastdifferentiation,aswellaschondrocytematuration,duringendochondralossification.

【 授权许可】

Unknown