TENDON CELLS--INTERACTIONS AND RESPONSES TO STRESS

肌腱细胞——相互作用和对压力的反应

• 批准号: 3158413
• 负责人: ALBERT J BANES
• 金额: $ 10.65万
• 依托单位: UNIV OF NORTH CAROLINA CHAPEL HILL
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-08-01 至 1990-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3158413
• 关键词: cell cell interaction; cell cycle; cell growth regulation; crosslink; exercise; fibroblasts; fluorescence microscopy; immobilization of body part; mechanical stress; synovial fluid; tendon injury; tendons; tissue /cell culture; vascular endothelium; wound healing

Tendon injuries, particularly sports-related injuries, constitute an increasing proportion of cases treated at our hospital, yet research in the molecular and cell biology of tendon healing is in its embryonic stages. Morphological, biomechanical and biochemical studies of normal tendon have revealed fundamental architecture, that exercise enhances healing and that fewer collagen crosslinks can be correlated with increased range of motion during convalescence after tendon injury. The overall objective of this study is to establish, on the molecular level, how exercise alters the metabolism of tendon cells to yield the proper balance between cell division and matrix production resulting in a healed tendon that is strong yet flexible. Results of recent experiments in this laboratory indicate that aortic endothelial cells respond to a repeating stress cycle of 10 sec 10% elongation and 10 sec relaxation in vitro by increasing their rate of division. The same stress regimen decreases the division rate of tendon fibroblasts. These different responses to the same stress field seem reasonable given that endothelial cells need to completely cover the interior of a blood vessel and regulate transport, but do not contribute much mechanical strength, whereas an organ such as tendon requires great tensile strength to transmit the force of muscle contraction to bone effect limb movement. In this case, if tendon became highly cellular, it would have insufficient mechanical strength to perform its work. Hence cyclic stress to tendon probably results in matrix production and not cell division. The important conclusion is that the response to physical stress probably varies for each tissue and may depend on the nature of the stress as well as the cell type affected. It should be possible to define what regimen activates a given cell to produce one of two principle effects: an alteration in cell division or matrix production. It is most likely that rapid changes in cells, occurring in secs or mins, could be involved in signal reception or transduction related to the magnitude of the stress. Slower responses involved in long term reactions would involve whether or not cells divide or produce matrix resulting in tissue build-up or degradation affecting the ultimate strength and flexibility of the tissue. In this proposal, I intend to correlate cell metabolism and matrix qualities of living tendon subjected to exercise or immobilization, the two extremes of applied force in vivo with those of cells subjected to applied force in vitro.

肌腱损伤，特别是与运动有关的损伤，构成 在我们医院接受治疗的病例比例不断上升，但 肌腱愈合的分子和细胞生物学研究进展 它的萌芽阶段。形态、生物力学和 对正常肌腱的生化研究揭示了 建筑，这种锻炼增强了治愈能力，而且更少 胶原蛋白交联物的增加与 肌腱损伤后恢复期的运动。整体而言 这项研究的目的是在分子水平上建立如何 运动改变肌腱细胞的新陈代谢，以产生适当的 细胞分裂和基质产生之间的平衡导致 愈合的肌腱，既结实又灵活。最近的结果 本实验室的实验表明，主动脉内皮细胞 细胞对10s 10%伸长的重复应力循环做出反应 和10秒的体外松弛，通过提高它们的分裂速度。 相同的应力训练方案降低了肌腱的分割率 成纤维细胞。这些对相同应力场的不同反应 考虑到内皮细胞需要完全 覆盖血管内部并调节运输，但确实如此 不会产生太大的机械强度，而像这样的器官 因为肌腱需要很大的抗拉强度才能传递 肌肉收缩到骨骼会影响肢体运动。在这种情况下，如果 肌腱变得高度细胞化，它将不足以 执行其工作所需的机械强度。因此循环应力为 肌腱可能导致基质产生，而不是细胞分裂。 重要的结论是，对身体压力的反应 可能因每种组织而异，并可能取决于 应力以及受影响的细胞类型。这应该是可能的 定义哪种方案激活给定的细胞以产生 两个主要影响：细胞分裂或基质的改变 制作。最有可能的是细胞的快速变化，发生在 秒或分钟，可能参与信号接收或 转导与压力的大小有关。速度较慢 长期反应中涉及的反应包括 或细胞不分裂或产生基质，导致组织堆积或 影响钢丝绳极限强度和灵活性的退化 组织。在这个提案中，我打算将细胞新陈代谢和 运动或运动状态下活肌腱的基质性质 固定，活体内作用力的两个极端 在体外受外力作用的细胞。