Hypoxic ADSCs-derived EVs promote the proliferation and chondrogenic differentiation of cartilage stem/progenitor cells.
Hypoxic ADSCs-derived EVs promote the proliferation and chondrogenic differentiation of cartilage stem/progenitor cells.
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缺氧的 ADSC 衍生的 EV 促进软骨干/祖细胞的增殖和软骨分化
DOI:
10.1080/21623945.2021.1945210
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发表时间:
2021-12
期刊:
影响因子:
3.3
通讯作者:
Liu K
中科院分区:
文献类型:
--
作者:
Xue K;Jiang Y;Zhang X;Wu J;Qi L;Liu K
ABSTRACT Cartilage tissue engineering is a promising option for repairing cartilage defects, although harvesting a large number of seeding cells remains a major challenge. Cartilage stem/progenitor cells (CSPCs) seem to be a promising cell source. Hypoxic extracellular vesicles (EVs) may play a major role in cell-cell and tissue-tissue communication. In the current study, we aimed to evaluate the effect of hypoxic adipose-derived stem cells (ADSCs)-derived EVs on CSPCs proliferation and differentiation. The characteristics of ADSCs-derived EVs were identified, and proliferation, migration, and cartilage-related gene expression of CSPCs were measured with or without the presence of hypoxic ADSCs-derived EVs. SEM, histological staining, biochemical and biomechanical analysis was performed to evaluate the effect of hypoxic ADSCs-derived EVs on CSPCs in alginate hydrogel culture. The results indicated that the majority of ADSC-derived EVs exhibited a round-shaped or cup-shaped morphology with a diameter of 40–1000 nm and expressed CD9, CD63, and CD81. CSPCs migration and proliferation were enhanced by hypoxic ADSCs-derived EVs, which also increased the expression of cartilage-related genes. The hypoxic ADSCs-derived EVs induce CSPCs to produce significantly more cartilage matrix and proteoglycan. In conclusion, hypoxic ADSCs-derived EVs improved the proliferation and chondrogenic differentiation of CSPCs for cartilage tissue engineering.
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DOI:
10.1073/pnas.1521230113
发表时间:
2016-02-23
影响因子:
11.1
作者:
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2.3
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4
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DOI:
10.1007/978-1-4939-6728-5_4
发表时间:
2017-01-01
期刊:
EXOSOMES AND MICROVESICLES: METHODS AND PROTOCOLS
影响因子:
--
作者:
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通讯作者:
Brisson, Alain R.