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基质压缩对关节软骨外植体中蛋白聚糖代谢的影响。

The effects of matrix compression on proteoglycan metabolism in articular cartilage explants.

作者信息

Guilak F, Meyer B C, Ratcliffe A, Mow V C

机构信息

Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, Columbia University, New York 10032, USA.

出版信息

Osteoarthritis Cartilage. 1994 Jun;2(2):91-101. doi: 10.1016/s1063-4584(05)80059-7.

Abstract

The effects of compressive stress on the rate of proteoglycan synthesis and release were determined in bovine articular cartilage from 4-5-month-old animals. Full depth cartilage explants were compressed in an unconfined configuration at various stresses ranging up to 1.0 MPa. At mechanical equilibrium (after 24 h), no significant changes were detected in the rate of [35S]-sulfate (35SO4) incorporation at the low level of compressive stresses used (less than 0.057 MPa). At an intermediate level of compressive stress (0.057, 0.1, 0.5 MPa), 35SO4 incorporation rates were reduced to approximately 60% of control values. At the highest level compressive stress (1.0 MPa) studied, 35SO4 incorporation rates were further reduced to approximately 20% that of controls. Recovery experiments at intermediate stress levels showed increased rates of 35SO4 incorporation at 24 h after compression. In explants loaded for 24 h at stresses of 0.1 MPa or higher, there was a stress-dose dependent inhibition of proteoglycan release into the media (up to 61% at 1.0 MPa), and proteoglycan release rates did not return to control values following a 24 h recovery period. While cartilage composition and biosynthetic activity were found to vary significantly with depth in control cartilage, the observed suppression (% change) in biosynthetic activity was relatively uniform with depth in both loading and recovery experiments. The study indicates that compression of the tissue to physiological strain magnitudes serves as a signal to modulate chondrocyte biosynthetic and catabolic responses through the depth of cartilage, while prolonged compression at higher strains may be responsible for tissue and cell damage.

摘要

研究了压缩应力对4 - 5月龄动物的牛关节软骨中蛋白聚糖合成和释放速率的影响。将全层软骨外植体在无侧限状态下以高达1.0 MPa的各种应力进行压缩。在机械平衡时(24小时后),在所使用的低水平压缩应力(小于0.057 MPa)下,未检测到[35S] - 硫酸盐(35SO4)掺入速率有显著变化。在中等水平的压缩应力(0.057、0.1、0.5 MPa)下,35SO4掺入速率降低至对照值的约60%。在所研究的最高水平压缩应力(1.0 MPa)下,35SO4掺入速率进一步降低至对照值的约20%。中等应力水平的恢复实验表明,压缩后24小时35SO4掺入速率增加。在0.1 MPa或更高应力下加载24小时的外植体中存在蛋白聚糖向培养基中释放的应力剂量依赖性抑制(在1.0 MPa时高达61%),并且在24小时恢复期后蛋白聚糖释放速率未恢复到对照值。虽然发现对照软骨的组成和生物合成活性随深度有显著变化,但在加载和恢复实验中,观察到的生物合成活性抑制(%变化)在深度上相对均匀。该研究表明,将组织压缩至生理应变幅度可作为一种信号,通过软骨深度调节软骨细胞的生物合成和分解代谢反应,而在较高应变下的长时间压缩可能导致组织和细胞损伤。

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