Sustained hypoxia enhances chondrocyte matrix synthesis.
Sustained hypoxia enhances chondrocyte matrix synthesis.
复制标题
DOI：
10.1002/jor.20816
复制
发表时间：
2009-06
期刊：
影响因子：
--
通讯作者：
Chu CR
中科院分区：
文献类型：
--
作者：
Coyle CH;Izzo NJ;Chu CR
关节软骨是一种无血管组织，在持续缺氧的条件下存在于较深层的软骨细胞。本研究使用缺氧室提供受控缺氧，以确定持续缺氧是否会增强软骨基质蛋白的产生。将新鲜分离的原代牛关节软骨细胞封装在三维藻酸盐珠中，并使用预平衡至 2% 氧气的培养基，在更换培养基时维持 2% 氧气。进行 HIF-1α 免疫定位以验证缺氧条件。仅 1 天后，持续缺氧就导致蛋白多糖合成增加（通过 35S-硫酸盐掺入测量）。在 17 天的研究期间，这种增加一直保持不变。缺氧培养 17 天后，通过间接免疫荧光、II 型胶原 ELISA 和实时 qPCR 检测总 II 型胶原和 COL2A1 基因表达的增加；此外，通过化学分析确定，观察到糖胺聚糖沉积增加。这些研究表明，持续缺氧可增强三维藻酸盐培养中的关节软骨细胞基质合成和活力。
Articular cartilage is an avascular tissue with chondrocytes in the deeper zones existing under conditions of sustained hypoxia. Using a hypoxic chamber to provide controlled hypoxia, this study was performed to determine whether sustained hypoxia enhances the production of cartilage matrix proteins. Freshly isolated primary bovine articular chondrocytes were encapsulated in three-dimensional alginate beads and maintained at 2% oxygen with media changes using media pre-equilibrated to 2% oxygen. Immunolocalization of HIF-1α was performed to verify hypoxic conditions. Sustained hypoxia resulted in an increase in proteoglycan synthesis after only 1 day, as measured by 35S-sulfate incorporation. This increase was maintained for the duration of the 17 day study. After 17 days of hypoxic culture, increases in total type II collagen and COL2A1 gene expression were probed by indirect immunofluorescence, type II collagen ELISA, and real-time qPCR; in addition, increased glycosaminoglycan deposition was observed as determined by chemical analysis. These studies show that sustained hypoxia enhances articular chondrocyte matrix synthesis and viability in three-dimensional alginate culture.
登录
查看更多内容
影响因子：
56.9
作者：
Jaakkola, P;Mole, DR;Ratcliffe, PJ
通讯作者：
Ratcliffe, PJ
影响因子：
7
作者：
Grimshaw, MJ;Mason, RM
通讯作者：
Mason, RM
影响因子：
4
作者：
Pfander, D;Cramer, T;Johnson, RS
通讯作者：
Johnson, RS
影响因子：
6.6
作者：
Iwata, Tomoyuki;Kawamoto, Takeshi;Kato, Yukio
通讯作者：
Kato, Yukio
影响因子：
2.6
作者：
Kawamura, K;Chu, CR;Niyibizi, C
通讯作者：
Niyibizi, C