Elucidation of the MAML-focused network system of hypertrophic differentiation in chondrocytes.

阐明软骨细胞肥大分化的以 MAML 为中心的网络系统。

• 批准号: 24659667
• 负责人: ONO Takashi
• 金额: $ 2.33万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24659667/
• 关键词: 軟骨細胞; 肥大分化; 軟骨分化; 軟骨細胞肥大分化; 変形性関節症

We checked the expression patterns of MAML family in mouse embryonic limb cartilage and found that MAML1 and MAML2 expressed in chondrocytes in hypertrophic zone. We further examined the expression patterns of MAML family by real-time RT-PCR during differentiation of cultured mouse chondrogenic cell line ATDC5 in the presence of insulin. The m-RNA levels of MAML1 and MAML2 were increased in their terminal differentiation stages. Overexression of MAML1 and MAML2 in ATDC5 cells and immature murine articular chondrocytes stimulated Mmp13 expression.

我们检测了MAML家族在小鼠胚胎肢体软骨中的表达模式，发现MAML1和MAML2在肥大区的软骨细胞中表达。我们进一步用实时定量RT-PCR检测了MAML家族在胰岛素存在下培养的小鼠软骨细胞系ATDC5分化过程中的表达模式。MAML1和MAML2的m-RNA水平在其终末分化阶段升高。MAML1和MAML2在ATDC5细胞和未成熟的小鼠关节软骨细胞中过表达可刺激MMP13的表达。