Department of Mechanical Engineering, University of California, Berkeley, CA, USA.
Department of Bioengineering, University of California, Berkeley, CA, USA.
Osteoarthritis Cartilage. 2024 May;32(5):548-560. doi: 10.1016/j.joca.2023.12.006. Epub 2023 Dec 30.
Cartilage tissue engineering strategies that use autologous chondrocytes require in vitro expansion of cells to obtain enough cells to produce functional engineered tissue. However, chondrocytes dedifferentiate during expansion culture, limiting their ability to produce chondrogenic tissue and their utility for cell-based cartilage repair strategies. The current study identified conditions that favor cartilage production and the mechanobiological mechanisms responsible for these benefits.
Chondrocytes were isolated from juvenile bovine knee joints and cultured with (primed) or without (unprimed) a growth factor cocktail. Gene expression, cell morphology, cell adhesion, cytoskeletal protein distribution, and cell mechanics were assessed. Following passage 5, cells were embedded into agarose hydrogels to evaluate functional properties of engineered cartilage.
Priming cells during expansion culture altered cell phenotype and chondrogenic tissue production. Unbiased ribonucleic acid-sequencing analysis suggested, and experimental studies confirmed, that growth factor priming delays dedifferentiation associated changes in cell adhesion and cytoskeletal organization. Priming also overrode mechanobiological pathways to prevent chondrocytes from remodeling their cytoskeleton to accommodate the stiff, monolayer microenvironment. Passage 1 primed cells deformed less and had lower yes associated protein 1 activity than unprimed cells. Differences in cell adhesion, morphology, and cell mechanics between primed and unprimed cells were mitigated by passage 5.
Priming suppresses mechanobiologic cytoskeletal remodeling to prevent chondrocyte dedifferentiation, resulting in more cartilage-like tissue-engineered constructs.
使用自体软骨细胞的软骨组织工程策略需要对细胞进行体外扩增,以获得足够的细胞来产生功能性工程组织。然而,软骨细胞在扩增培养过程中去分化,限制了其产生软骨组织的能力及其在基于细胞的软骨修复策略中的应用。本研究确定了有利于软骨生成的条件和负责这些益处的机械生物学机制。
从小牛膝关节中分离软骨细胞,并在有(预培养)或没有(未预培养)生长因子鸡尾酒的情况下培养。评估基因表达、细胞形态、细胞黏附、细胞骨架蛋白分布和细胞力学。在第 5 代后,将细胞嵌入琼脂糖水凝胶中,以评估工程软骨的功能特性。
在扩增培养过程中对细胞进行预培养会改变细胞表型和软骨组织的产生。无偏核糖核酸测序分析表明,实验研究证实,生长因子预培养会延迟与去分化相关的细胞黏附和细胞骨架组织改变。预培养还推翻了机械生物学途径,以防止软骨细胞重塑其细胞骨架以适应坚硬的单层微环境。第 1 代预培养的细胞比未预培养的细胞变形程度更小,Yes 相关蛋白 1 的活性更低。预培养和未预培养细胞之间的细胞黏附、形态和细胞力学差异在第 5 代时得到缓解。
预培养抑制机械生物学细胞骨架重塑,以防止软骨细胞去分化,从而产生更类似软骨的组织工程构建体。