国际口腔医学杂志
國際口腔醫學雜誌
국제구강의학잡지
JOURNAL OF INTERNATIONAL STOMATOLOGY
2015年
5期
615-619
,共5页
软骨内成骨%生物力%印第安刺猬蛋白%核心结合因子-α1%血管内皮细胞生长因子
軟骨內成骨%生物力%印第安刺猬蛋白%覈心結閤因子-α1%血管內皮細胞生長因子
연골내성골%생물력%인제안자위단백%핵심결합인자-α1%혈관내피세포생장인자
endochondral ossification%mechanical stress%Indian hedgehog%corebindingfactor-α1%vascular endothelial growth factor
软骨内成骨是一个复杂有序的生物学过程，依赖于一系列力敏感因子的精确调控，而生物力影响着软骨内成骨中力敏感因子的表达。对软骨细胞施加力学刺激后，印第安刺猬蛋白（IHH）表达增加，细胞增殖加快。IHH通过与甲状旁腺素-甲状旁腺素相关肽（PTHrP）受体形成的负反馈环路协调软骨细胞的增殖、成熟与分化，而IHH在调控软骨细胞增殖分化方面并非是PTHrP依赖性的。核心结合因子-α1不仅在软骨形成中，亦在血管侵入软骨过程中发挥作用，可刺激肥大软骨细胞中的血管内皮生长因子（VEGF）诱导血管侵入，促进软骨内骨化。VEGFA通过刺激内皮细胞的增殖和迁徙增加血管的通透性，而肥大软骨细胞基质降解、血管侵入是软骨内成骨的关键。VEGF在软骨内成骨过程中协调着软骨细胞增殖、破骨细胞功能、细胞外基质改建、血管增生和骨形成间的关系。生物力影响着软骨内成骨力敏感因子的表达，进而影响着软骨内成骨进程，理解其中的分子机制将有利于骨形成和骨修复研究。
軟骨內成骨是一箇複雜有序的生物學過程，依賴于一繫列力敏感因子的精確調控，而生物力影響著軟骨內成骨中力敏感因子的錶達。對軟骨細胞施加力學刺激後，印第安刺猬蛋白（IHH）錶達增加，細胞增殖加快。IHH通過與甲狀徬腺素-甲狀徬腺素相關肽（PTHrP）受體形成的負反饋環路協調軟骨細胞的增殖、成熟與分化，而IHH在調控軟骨細胞增殖分化方麵併非是PTHrP依賴性的。覈心結閤因子-α1不僅在軟骨形成中，亦在血管侵入軟骨過程中髮揮作用，可刺激肥大軟骨細胞中的血管內皮生長因子（VEGF）誘導血管侵入，促進軟骨內骨化。VEGFA通過刺激內皮細胞的增殖和遷徙增加血管的通透性，而肥大軟骨細胞基質降解、血管侵入是軟骨內成骨的關鍵。VEGF在軟骨內成骨過程中協調著軟骨細胞增殖、破骨細胞功能、細胞外基質改建、血管增生和骨形成間的關繫。生物力影響著軟骨內成骨力敏感因子的錶達，進而影響著軟骨內成骨進程，理解其中的分子機製將有利于骨形成和骨脩複研究。
연골내성골시일개복잡유서적생물학과정，의뢰우일계렬력민감인자적정학조공，이생물력영향착연골내성골중력민감인자적표체。대연골세포시가역학자격후，인제안자위단백（IHH）표체증가，세포증식가쾌。IHH통과여갑상방선소-갑상방선소상관태（PTHrP）수체형성적부반궤배로협조연골세포적증식、성숙여분화，이IHH재조공연골세포증식분화방면병비시PTHrP의뢰성적。핵심결합인자-α1불부재연골형성중，역재혈관침입연골과정중발휘작용，가자격비대연골세포중적혈관내피생장인자（VEGF）유도혈관침입，촉진연골내골화。VEGFA통과자격내피세포적증식화천사증가혈관적통투성，이비대연골세포기질강해、혈관침입시연골내성골적관건。VEGF재연골내성골과정중협조착연골세포증식、파골세포공능、세포외기질개건、혈관증생화골형성간적관계。생물력영향착연골내성골력민감인자적표체，진이영향착연골내성골진정，리해기중적분자궤제장유리우골형성화골수복연구。
Endochondral?ossification?is?a?complex?and?ordered?biological?process?that?is?precisely?regulated?by?many?force-sensitive?factors.?However,?biomechanical?agents?affect?the?expression?of?these?factors.?The?expression?of?Indian?hedgehog(IHH)?improved?after?mechanical?force?stimulation?was?applied?to?the?chondrocyte,?and?cell?proliferation?was?promoted.?IHH?coordinates?the?proliferation,?maturation,?and?differentiation?of?the?chondrocyteby?forming?a?negative?feedback?loop?with?parathyroid?hormone?related?protein(PTHrP).?Moreover,?IHH?is?necessary?for?chondrocyte?proliferation?anddifferentiationinapathwaythatcannotbedependentonPTHrP.Corebindingfactor-α1playsanimportantrolenot?only?in?the?chondrogenesis?but?also?in?the?process?of?vascular?invasion,?thereby?inducing?vascular?invasion?and?endochondral?ossification?by?stimulating?the?expression?of?vascular?endothelial?growth?factor(VEGF)?in?hypertrophic?chondrocytes.?VEGFA?improves?the?permeability?of?blood?vessels?by?stimulating?the?proliferation?and?migration?of?endothelial?cells.?Meanwhile,?the?matrix?degradation?of?hypertrophic?chondrocytes?and?blood?vessels?is?key?to?endochondral?ossification.?VEGF?coordinates?the?relationship?of?chondrocyte?proliferation,?osteoclast?function,?extracellular?matrix?rebuilding,?vascular?proliferation,?and?bone?formation.?Biomechanical?agents?affect?the?expression?of?force-sensitive?factors?and?the?progress?of?endochondral?ossification.?Understanding?the?molecular?mechanism?underlying?the?abovementioned?phenomenon?will?benefit?our?research?onbone?formation?and?repair.
