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首页> 外文期刊>Biotechnology Progress >Scaffoldless tissue-engineered cartilage for studying transforming growth factor beta-mediated cartilage formation
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Scaffoldless tissue-engineered cartilage for studying transforming growth factor beta-mediated cartilage formation

机译：用于研究转化生长因子β介导的软骨形成的脚腰组织工程软骨

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Reduced transforming growth factor beta (TGF-beta) signaling is associated with osteoarthritis (OA). TGF-beta is thought to act as a chondroprotective agent and provide anabolic cues to cartilage, thus acting as an OA suppressor in young, healthy cartilage. A potential approach for treating OA is to identify the factors that act downstream of TGF-beta's anabolic pathway and target those factors to promote cartilage regeneration or repair. The aims of the present study were to (a) develop a scaffoldless tissue-engineered cartilage model with reduced TGF-beta signaling and disrupted cartilage formation and (b) validate the system for identifying the downstream effectors of TGF-beta that promote cartilage formation. Sox9 was used to validate the model because Sox9 is known to promote cartilage formation and TGF-beta regulates Sox9 activity. Primary bovine articular chondrocytes were grown in Transwell supports to form cartilage tissues. An Alk5/TGF-beta type I receptor inhibitor, SB431542, was used to attenuate TGF-beta signaling, and an adenovirus encoding FLAG-Sox9 was used to drive the expression of Sox9 in the in vitro-generated cartilage. SB431542-treated tissues exhibited reduced cartilage formation including reduced thicknesses and reduced proteoglycan staining compared with control tissue. Expression of FLAG-Sox9 in SB431542-treated cartilage allowed the formation of cartilage despite antagonism of the TGF-beta receptor. In summary, we developed a three-dimensional in vitro cartilage model with attenuated TGF-beta signaling. Sox9 was used to validate the model for identification of anabolic agents that counteract loss of TGF-beta signaling. This model has the potential to identify additional anabolic factors that could be used to repair or regenerate damaged cartilage.
机译：转化生长因子β（TGF-β）信号传导降低与骨关节炎（OA）有关。 TGF-β被认为是作为软骨，并为软骨提供合成代谢性提示，从而作为年轻，健康的软骨中的OA抑制剂。治疗OA的潜在方法是识别在TGF-β的合成型途径下游起作用的因素，并针对这些因素来促进软骨再生或修复。本研究的目的是（a）开发具有降低的TGF-β信号传导和破坏的软骨形成和（b）验证促进软骨形成的TGF-β的下游效应器的系统。 SOX9用于验证模型，因为已知SOX9促进软骨形成和TGF-β调节SOX9活性。原发性牛关节软骨细胞在Transwell载体中生长以形成软骨组织。 ALK5 / TGF-β型I受体抑制剂SB431542用于衰减TGF-β信号传导，并且使用腺病毒编码标志-SOX9用于在体外产生的软骨中驱动SOX9的表达。 SB431542处理的组织表现出降低的软骨形成，包括减少厚度和与对照组织相比的蛋白质增生染色染色。尽管TGF-β受体拮抗，但SB431542治疗的软骨中的标志-SOx9的表达允许形成软骨。总之，我们开发了具有衰减TGF-Beta信号的三维体外软骨模型。 SOX9用于验证鉴定抵消TGF-Beta信号传导损失的合成代谢剂的模型。该模型有可能识别可用于修复或再生受损软骨的额外的合成代谢因素。

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