Microfluidics-based optimization of neuroleukin-mediated regulation of articular chondrocyte proliferation

Microfluidics-based optimization of neuroleukin-mediated regulation of articular chondrocyte proliferation
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基于微流体的神经白介素介导的关节软骨细胞增殖调节的优化

DOI:
10.3892/mmr.2015.4540
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发表时间:
2015-11
影响因子:
3.4
通讯作者:
Liu Han
Liu Han
中科院分区:
医学4区
文献类型:
--
作者:
Tian Kang;Zhong Weiliang;Zhang Yingqiu;Yin Baosheng;Zhang Weiguo;Liu Han

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由于软骨细胞的增殖和迁移能力低,软骨修复仍然是一个具有挑战性的临床问题。目前软骨修复的治疗策略导致不令人满意的结果。自体软骨细胞植入(ACI)是一种基于细胞的疗法,依赖于患者健康软骨细胞的体外扩增,在此期间经常使用增殖促进因子。神经白细胞介素(NLK)是一种具有生长因子功能的多功能蛋白质,其表达与软骨发育和骨再生有关,但其在软骨细胞增殖中的直接作用尚未完全阐明。在本研究中,除了其在ACI期间作为外源性因子的潜力外,还研究了NLK在体外软骨细胞增殖中的作用。此外,使用微流体装置优化用于体外软骨细胞培养的NLK浓度。观察到12.85 ng/ml的NLK浓度为促进软骨细胞增殖提供了最佳条件。此外,NLK刺激导致软骨细胞II型胶原合成增加,这是一种软骨分泌标志物,与软骨细胞的表型相关。总之,这些数据表明,NLK是能够促进细胞增殖和II型胶原蛋白的合成在体外软骨细胞繁殖,因此可以作为一个外源性因子ACI。
Due to the low proliferative and migratory capacities of chondrocytes, cartilage repair remains a challenging clinical problem. Current therapeutic strategies for cartilage repair result in unsatisfactory outcomes. Autologous chondrocyte implantation (ACI) is a cell based therapy that relies on the in vitro expansion of healthy chondrocytes from the patient, during which proliferation-promoting factors are frequently used. Neuroleukin (NLK) is a multifunctional protein that possesses growth factor functions, and its expression has been associated with cartilage development and bone regeneration, however its direct role in chondrocyte proliferation remains to be fully elucidated. In the current study, the role of NLK in chondrocyte proliferation in vitro in addition to its potential to act as an exogenous factor during ACI was investigated. Furthermore, the concentration of NLK for in vitro chondrocyte culture was optimized using a microfluidic device. An NLK concentration of 12.85 ng/ml was observed to provide optimal conditions for the promotion of chondrocyte proliferation. Additionally, NLK stimulation resulted in an increase in type II collagen synthesis by chondrocytes, which is a cartilaginous secretion marker and associated with the phenotype of chondrocytes. Together these data suggest that NLK is able to promote cell proliferation and type II collagen synthesis during in vitro chondrocyte propagation, and thus may serve as an exogenous factor for ACI.
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