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Article Open Access

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

  • Authors:
    • Kang Tian
    • Weiliang Zhong
    • Yingqiu Zhang
    • Baosheng Yin
    • Weiguo Zhang
    • Han Liu
  • View Affiliations / Copyright

    Affiliations: Department of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China
    Copyright: © Tian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 67-74
    |
    Published online on: November 10, 2015
       https://doi.org/10.3892/mmr.2015.4540
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Abstract

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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Copy and paste a formatted citation
Spandidos Publications style
Tian K, Zhong W, Zhang Y, Yin B, Zhang W and Liu H: Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation. Mol Med Rep 13: 67-74, 2016.
APA
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., & Liu, H. (2016). Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation. Molecular Medicine Reports, 13, 67-74. https://doi.org/10.3892/mmr.2015.4540
MLA
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., Liu, H."Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation". Molecular Medicine Reports 13.1 (2016): 67-74.
Chicago
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., Liu, H."Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation". Molecular Medicine Reports 13, no. 1 (2016): 67-74. https://doi.org/10.3892/mmr.2015.4540
Copy and paste a formatted citation
x
Spandidos Publications style
Tian K, Zhong W, Zhang Y, Yin B, Zhang W and Liu H: Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation. Mol Med Rep 13: 67-74, 2016.
APA
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., & Liu, H. (2016). Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation. Molecular Medicine Reports, 13, 67-74. https://doi.org/10.3892/mmr.2015.4540
MLA
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., Liu, H."Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation". Molecular Medicine Reports 13.1 (2016): 67-74.
Chicago
Tian, K., Zhong, W., Zhang, Y., Yin, B., Zhang, W., Liu, H."Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation". Molecular Medicine Reports 13, no. 1 (2016): 67-74. https://doi.org/10.3892/mmr.2015.4540
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