Sánchez Julio C, López-Zapata Diego F
Grupo de Fisiología Celular y Aplicada, Facultad Ciencias de la Salud, Universidad Tecnológica de Pereira, Pereira, Risaralda, Colombia.
Biorheology. 2010;47(5-6):321-31. doi: 10.3233/BIR-2010-0577.
Changes in external osmolarity arise from variations in mechanical loads on joints and may affect the homeostasis of chondrocytes, which are the only cell type responsible for matrix turnover. Accordingly, variations in membrane potential may affect cartilage production. The present study assessed the effects of variations in external osmolarity on membrane potential and the possible mechanisms responsible for this response. Membrane potential was measured by the patch clamp whole-cell technique using human articular chondrocytes freshly isolated from healthy and osteoarthritic cartilage. The membrane potential was -39±4 mV in articular human chondrocytes from healthy cartilage and -26±4 mV in those from osteoarthritic cartilage. Increasing the osmolarity produced a reversible hyperpolarization mediated by K+ efflux through BKCa channels in both groups of chondrocytes, but the response in osteoarthritic cells was significantly reduced; no other K+ pathways were involved in this effect. Alternatively, decreasing the osmolarity elicited depolarization in healthy chondrocytes but did not produce any response in chondrocytes from osteoarthritic cartilage. The depolarization was dependent on Na+ influx through Gd3+-sensitive stretch-activated cation channels and was independent of external Ca2+. The differential responses observed in chondrocytes from osteoarthritic cartilage suggest that disregulation on the responses to external osmolarity may be involved in the process that leads to the alterations in the cartilage structure observed in osteoarthritis.
外部渗透压的变化源于关节机械负荷的改变，可能会影响软骨细胞的稳态，而软骨细胞是唯一负责基质更新的细胞类型。因此，膜电位的变化可能会影响软骨生成。本研究评估了外部渗透压变化对膜电位的影响以及导致这种反应的可能机制。使用从健康和骨关节炎软骨中新鲜分离的人关节软骨细胞，通过膜片钳全细胞技术测量膜电位。健康软骨的人关节软骨细胞的膜电位为-39±4 mV，骨关节炎软骨的人关节软骨细胞的膜电位为-26±4 mV。在两组软骨细胞中，渗透压升高均通过BKCa通道介导的K+外流产生可逆性超极化，但骨关节炎细胞中的反应明显减弱；该效应不涉及其他K+途径。相反，渗透压降低在健康软骨细胞中引起去极化，但在骨关节炎软骨的软骨细胞中未产生任何反应。去极化依赖于通过Gd3+敏感的牵张激活阳离子通道的Na+内流，且与细胞外Ca2+无关。在骨关节炎软骨的软骨细胞中观察到的差异反应表明，对外部渗透压反应的失调可能参与了导致骨关节炎中观察到的软骨结构改变的过程。
