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Background <p>Osteoarthritis (OA) is a commonly occurring degenerative joint disorder. Presently, primary clinical interventions, including nonsteroidal anti-inflammatory drugs (NSAIDs), primarily provide symptomatic alleviation. Glutamine (Gln) has been shown to have protective effects on chondrocytes, which may postpone OA progression. Nevertheless, its effectiveness in the ATDC5 chondrogenic cell line has yet to be explored.</p> Objective <p>The objective of this research was to explore the ability of Gln to increase the proliferation and chondrogenic differentiation of ATDC5 cells and to clarify the underlying molecular mechanisms.</p> Methods <p>The murine ATDC5 cell line was maintained in culture, and an in vitro OA model was developed through the application of interleukin-1 beta (IL-1β). The therapeutic effects of Gln were investigated. Cell proliferation was assessed using the CCK-8 assay. The levels of inflammatory mediators and matrix metalloproteinases (MMPs) were measured using Western blot analysis. The expression of chondrogenic markers, including SOX9, aggrecan, and collagen type II (collagen Ⅱ), were also evaluated via Western blotting. A transcriptomic analysis was conducted to identify differentially expressed genes (DEGs) and their related signalling pathways. The crucial molecules involved in these pathways were subsequently validated through Western blot and immunofluorescence techniques.</p> Results <p>In vitro studies revealed that at concentrations of 5 mM, 10 mM, and 20 mM, Gln markedly increased the proliferation of ATDC5 cells, with the effect occurring most strongly at a concentration of 10mM. Notably, Gln concentrations as high as 80mM did not exhibit any cytotoxic effects. Additionally, treatment with 10 mM Gln significantly reduced the expression of inflammatory mediators and matrix metalloproteinases (MMPs) induced by IL-1β. This concentration also promoted the upregulation of key cartilage markers, including aggrecan, collagen II, and SOX9, while significantly decreasing apoptosis in ATDC5 cells. These protective effects appear to be linked to the inhibition of the PI3K-AKT signalling pathway.</p> Conclusion <p>Glutamine alleviates cell injury induced by interleukin-1 beta (IL-1β) by suppressing apoptosis, extracellular matrix breakdown, and inflammatory reactions in ATDC5 cells. Moreover, Gln enhances cell proliferation and promotes chondrogenic differentiation. The observed therapeutic effects seem to operate through the downregulation of the PI3K-AKGT signalling pathway.</p>

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Role of glutamine in promoting the proliferation and chondrogenic differentiation of ATDC5 cells: based on transcriptomic analysis

  • 期刊论文

  • 发表日期：

    2026年3月12日

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  • Rui-hao Zhang,
  • Wen-huan Yuan,
  • Ze-long Wang,
  • Qi-rui Yang,
  • Yi Sun,
  • Quan-nian Shao,
  • Wen-ji Wang,
  • Jing Wang

摘要

Background

Osteoarthritis (OA) is a commonly occurring degenerative joint disorder. Presently, primary clinical interventions, including nonsteroidal anti-inflammatory drugs (NSAIDs), primarily provide symptomatic alleviation. Glutamine (Gln) has been shown to have protective effects on chondrocytes, which may postpone OA progression. Nevertheless, its effectiveness in the ATDC5 chondrogenic cell line has yet to be explored.

Objective

The objective of this research was to explore the ability of Gln to increase the proliferation and chondrogenic differentiation of ATDC5 cells and to clarify the underlying molecular mechanisms.

Methods

The murine ATDC5 cell line was maintained in culture, and an in vitro OA model was developed through the application of interleukin-1 beta (IL-1β). The therapeutic effects of Gln were investigated. Cell proliferation was assessed using the CCK-8 assay. The levels of inflammatory mediators and matrix metalloproteinases (MMPs) were measured using Western blot analysis. The expression of chondrogenic markers, including SOX9, aggrecan, and collagen type II (collagen Ⅱ), were also evaluated via Western blotting. A transcriptomic analysis was conducted to identify differentially expressed genes (DEGs) and their related signalling pathways. The crucial molecules involved in these pathways were subsequently validated through Western blot and immunofluorescence techniques.

Results

In vitro studies revealed that at concentrations of 5 mM, 10 mM, and 20 mM, Gln markedly increased the proliferation of ATDC5 cells, with the effect occurring most strongly at a concentration of 10mM. Notably, Gln concentrations as high as 80mM did not exhibit any cytotoxic effects. Additionally, treatment with 10 mM Gln significantly reduced the expression of inflammatory mediators and matrix metalloproteinases (MMPs) induced by IL-1β. This concentration also promoted the upregulation of key cartilage markers, including aggrecan, collagen II, and SOX9, while significantly decreasing apoptosis in ATDC5 cells. These protective effects appear to be linked to the inhibition of the PI3K-AKT signalling pathway.

Conclusion

Glutamine alleviates cell injury induced by interleukin-1 beta (IL-1β) by suppressing apoptosis, extracellular matrix breakdown, and inflammatory reactions in ATDC5 cells. Moreover, Gln enhances cell proliferation and promotes chondrogenic differentiation. The observed therapeutic effects seem to operate through the downregulation of the PI3K-AKGT signalling pathway.