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Background <p>Major depressive disorder (MDD) is a highly prevalent psychiatric disorder and one of the leading causes of disability worldwide. Neuroinflammation is strongly implicated in the pathophysiology of MDD, suggesting that regulators of neuroinflammatory signaling are feasible therapeutic targets. The <i>CTNND1</i> gene encodes a member of the armadillo protein family termed p120 (or catenin delta) that functions in cell–cell adhesion and signal transduction, including among immune cells, suggesting immunomodulatory activity.</p> Results <p>We report that systemic injection of the bacterial toxin lipopolysaccharide (LPS) induced depression-like behaviors in mice while concomitantly activating the neuroinflammatory NF-κB signaling pathway, upregulating interleukin (IL)-1β expression, and reducing p120 expression in the hippocampus. Moreover, shRNA-mediated knockdown of hippocampal p120 expression also activated the NF-κB signaling pathway, enhanced IL-1β expression, and induced the same depression-like behaviors. Similarly, both LPS treatment and p120 knockdown upregulated pNF-κB and IL-1β levels in pheochromocytoma-12 cells.</p> Conclusions <p>These findings suggest that p120 may function to prevent the development or expression of depressive symptoms by suppressing proinflammatory NF-κB-IL-1β signaling in the hippocampus. Targeting p120 may be a feasible therapeutic strategy to treat MDD.</p> Graphical Abstract <p>Knockdown of p120 serve as a negative regulator of neuroinflammation via NF-κB signalling.</p> <p></p>

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Downregulation of p120 catenin in the mouse hippocampus contributes to the development of depression-like phenotypes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Chen Chen,
  • Lai-peng Feng,
  • Pei-ling Shi,
  • Qing Liu,
  • Lu-wen Zhang,
  • Qi Wang,
  • Rui-fang Hua,
  • Xi Su,
  • Wen-qiang Li

摘要

Background

Major depressive disorder (MDD) is a highly prevalent psychiatric disorder and one of the leading causes of disability worldwide. Neuroinflammation is strongly implicated in the pathophysiology of MDD, suggesting that regulators of neuroinflammatory signaling are feasible therapeutic targets. The CTNND1 gene encodes a member of the armadillo protein family termed p120 (or catenin delta) that functions in cell–cell adhesion and signal transduction, including among immune cells, suggesting immunomodulatory activity.

Results

We report that systemic injection of the bacterial toxin lipopolysaccharide (LPS) induced depression-like behaviors in mice while concomitantly activating the neuroinflammatory NF-κB signaling pathway, upregulating interleukin (IL)-1β expression, and reducing p120 expression in the hippocampus. Moreover, shRNA-mediated knockdown of hippocampal p120 expression also activated the NF-κB signaling pathway, enhanced IL-1β expression, and induced the same depression-like behaviors. Similarly, both LPS treatment and p120 knockdown upregulated pNF-κB and IL-1β levels in pheochromocytoma-12 cells.

Conclusions

These findings suggest that p120 may function to prevent the development or expression of depressive symptoms by suppressing proinflammatory NF-κB-IL-1β signaling in the hippocampus. Targeting p120 may be a feasible therapeutic strategy to treat MDD.

Graphical Abstract

Knockdown of p120 serve as a negative regulator of neuroinflammation via NF-κB signalling.