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Purpose <p>Pulmonary hypertension is a serious pulmonary vascular disease. During the course of development, pulmonary artery smooth muscle cells (PASMCs) exhibit hyperplasia, enhanced anti-apoptotic effect, cell deformation, and migration. S100A4 protein is a member of the S100 protein family, which can deform and migrate arterial smooth muscle cells. Pulmonary hypertension can increase S100A4 protein expression. However, the underlying mechanism by which S100A4 is involved in the progression of pulmonary hypertension remains unclear.</p> Methods <p>In this study, the effects of recombinant human S100A4 protein treatment on cell proliferation, migration, and Fibulin-5 expression, as well as the effects of Fibulin-5 interference on cell proliferation and migration, were evaluated in human PASMCs. Subsequently, the impact of Fibulin-5 interference on cell proliferation and migration following recombinant human S100A4 protein treatment was investigated.</p> Results <p>It was demonstrated that exogenous S100A4 upregulated Fibulin-5 expression, thereby promoted PASMC proliferation. Conversely, Fibulin-5 interference was found to reverse the effects of Re-S100A4.</p> Conclusion <p>This study further complements and improves the mechanism network related to pulmonary hypertension, thereby demonstrating that S100A4 and Fibulin-5 may become a new target for clinical intervention in pulmonary hypertension.</p>

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The mechanism of S100A4 regulating Fibulin-5 expression to promote the proliferation and migration of PASMCs

  • 期刊论文

  • 发表日期：

    2026年4月2日

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  • Bingzhu Hu,
  • Shi Chen,
  • Lixia Dong

摘要

Purpose

Pulmonary hypertension is a serious pulmonary vascular disease. During the course of development, pulmonary artery smooth muscle cells (PASMCs) exhibit hyperplasia, enhanced anti-apoptotic effect, cell deformation, and migration. S100A4 protein is a member of the S100 protein family, which can deform and migrate arterial smooth muscle cells. Pulmonary hypertension can increase S100A4 protein expression. However, the underlying mechanism by which S100A4 is involved in the progression of pulmonary hypertension remains unclear.

Methods

In this study, the effects of recombinant human S100A4 protein treatment on cell proliferation, migration, and Fibulin-5 expression, as well as the effects of Fibulin-5 interference on cell proliferation and migration, were evaluated in human PASMCs. Subsequently, the impact of Fibulin-5 interference on cell proliferation and migration following recombinant human S100A4 protein treatment was investigated.

Results

It was demonstrated that exogenous S100A4 upregulated Fibulin-5 expression, thereby promoted PASMC proliferation. Conversely, Fibulin-5 interference was found to reverse the effects of Re-S100A4.

Conclusion

This study further complements and improves the mechanism network related to pulmonary hypertension, thereby demonstrating that S100A4 and Fibulin-5 may become a new target for clinical intervention in pulmonary hypertension.