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丝裂原活化蛋白激酶通路在髁突软骨细胞力学信号转导过程中的作用
引用本文:张旻,王美青,王景杰. 丝裂原活化蛋白激酶通路在髁突软骨细胞力学信号转导过程中的作用[J]. 上海口腔医学, 2004, 13(6): 510-514
作者姓名:张旻  王美青  王景杰
作者单位:第四军医大学口腔医学院,解剖生理教研室,陕西,西安,710032;第四军医大学口腔医学院,牙体病科,陕西,西安,710032
基金项目:国家自然科学基金(30000035)
摘    要:目的:探讨丝裂原活化蛋白激酶(MAPK)家族中细胞外调节蛋白激酶1(ERK1)和c-JunN末端激酶1(JNK1)的表达和分布以及随压力环境的变化过程。方法:体外培养髁突软骨细胞,采用可控液压细胞加载装置,在90kPa压强下分别加载60min、360min,Western印迹杂交法检测ERK1和JNK1蛋白表达水平;免疫组化染色观察加压前后ERK1和JNK1的分布变化。结果:90kPa加压60min及90kPa加压360min后,髁突软骨细胞(MCC)中ERK1含量分别较对照组升高73.21%±1.28%和32.57%±1.43%(P<0.01),在90kPa压力刺激后60min表达水平最高,并伴随向细胞核内的转位;而JNK1的含量分别较对照组升高38.24%±1.38%和83.74%±1.52%(P<0.01),在90kPa刺激360min后表达水平最高,也同时伴有由细胞质向胞核的转位。结论:MAPK途径是髁突软骨细胞力学信号转导过程中的重要通路,适宜的压力刺激可导致ERK和JNK/SAPK表达增强及由细胞质向胞核的转位。

关 键 词:髁突软骨细胞  压力  丝裂原活化蛋白激酶
文章编号:1006-7248(2004)06-0510-05
修稿时间:2004-02-06

The role of the MAPK pathway in mandibular condylar chondrocytes mechanotransduction
ZHANG Min,WANG Mei-qing,WANG Jing-jie.. The role of the MAPK pathway in mandibular condylar chondrocytes mechanotransduction[J]. Shanghai journal of stomatology, 2004, 13(6): 510-514
Authors:ZHANG Min  WANG Mei-qing  WANG Jing-jie.
Affiliation:Department of Oral Anatomy and Physiology, School of Stomatology, Fourth Military Medical University, Xi'an 710032, Shanxi Providence, China. zhangmin@fmmu.edu.cn
Abstract:PURPOSE: To investigate the expression and distribution of extracellular-regulated protein kinase (ERK) and c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) under the mechanical pressure in rabbit mandibular condylar chondrocytes (MCC). METHODS: In vitro cultured MCC from two-week-old New Zealand rabbits were incubated. Under continuous pressure of 90 kPa for 60 minutes and 360 minutes by hydraulic pressure controlled cellular strain unit, the expression of ERK1 and JNK1 were evaluated by Western blot analyses. The distributions of them were observed by immunocytochemical staining. RESULTS: The expression of ERK1 increased by 73.21%+/-1.28% under the pressure of 90 kPa for 60 minutes and 32.57%+/-1.43% under the pressure of 90 kPa for 360 minutes (P<0.01)respectively. But that of JNK1 reached the highest till 360 minutes. And the expression of it increased by 38.24%+/-1.38% under the pressure of 90 kPa for 60 minutes and 83.74%+/-1.52% for 360 minutes (P<0.01). Under the pressure, the distribution of both ERK1 and JNK1 showed translocation from cytoplasm to nuclei. CONCLUSIONS: MAPK pathway is an important access for MCC mechanotransduction. Feasible pressure could promote the expression and translocation of both ERK1 and JNK1.
Keywords:Mandibular condylar chondrocytes (MCC)  Mechanical pressure  Mitogen-activated protein kinases ( MAPK)
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