TY - JOUR A2 - 长安，鹏AU - 甘，薄一波AU - 恩，兵AU - 李，裴非盟 - 叶，吉星AU - 赵，陈AU - 洛，雷AU - 张，承敏AU - 张，Zetong AU -朱，林勇AU - 周蔷PY - 2018 DA - 2018年4月17日TI - 7061898 VL - - 2018 AB - 间充质干骨髓间充质通过TRPV4依赖途径SP干向髓核细胞的细胞压缩增强生物合成的低幅度细胞（MSC-）为基础的治疗被认为是有希望的组织工程策略来实现髓核（NP）为再生椎间盘退行性变（IDD）的治疗。但是，它仍然是促进MSC的生物合成，以满足NP再生的需求的挑战。本研究的目的是优化的压缩幅度，以增强向MSC的discogenesis细胞外基质（ECM）沉积。Thus, we constructed a 3D culture model for MSCs to bear different magnitudes of compression for 7 days (5%, 10%, and 20% at the frequency of 1.0 Hz for 8 hours/day) using an intelligent and mechanically active bioreactor. Then, the underlying mechanotransduction mechanism of transient receptor potential vanilloid 4 (TRPV4) was further explored. The MSC-encapsulated hybrids were evaluated by Live/Dead staining, biochemical content assay, real-time PCR, Western blot, histological, and immunohistochemical analysis. The results showed that low-magnitude compression promoted anabolic response where high-magnitude compression induced the catabolic response for the 3D-cultured MSCs. The anabolic effect of low-magnitude compression could be inhibited by inhibiting TRPV4. Meanwhile, the activation of TRPV4 enhanced the biosynthesis analogous to low-magnitude compression. These findings demonstrate that low-magnitude compression promoted the anabolic response of ECM deposition towards discogenesis for the 3D-cultured MSCs and the TRPV4 channel plays a key role on mechanical signal transduction for low-magnitude compressive loading. Further understanding of this mechanism may provide insights into the development of new therapies for MSC-based NP regeneration. SN - 1687-966X UR - https://doi.org/10.1155/2018/7061898 DO - 10.1155/2018/7061898 JF - Stem Cells International PB - Hindawi KW - ER -