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<p>Pulmonary hypertension (PH) is associated with fluid shear stress (FSS) and Gremlin1 (Grem1), but the mechanism by which FSS acts on Grem1 remains unclear. Here we found that FSS downregulated Grem1 in bEnd.3 cells. Meanwhile, FSS inhibited the expression of transcription factor EGR1. Mechanistically, FSS inhibited the transcriptional activity of Grem1 promoter by down-regulating EGR1. RNA-seq and cell function analysis indicated that FSS inhibited the cell cycle and proliferation through the EGR1/Grem1 axis in bEnd.3 cells. In addition, FSS also down-regulated the expression of Grem1 and EGR1 in mouse/rat pulmonary microvascular endothelial cells. Together, our findings revealed the mechanism by which FSS inhibited the cell cycle and proliferation of vascular endothelial cells through the EGR1/Grem1 axis, providing new insights into the development of PH.</p>

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Fluid shear stress inhibits vascular endothelial cells proliferation via EGR1/Grem1 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Zhiqiang Zha,
  • Fangjian He,
  • Yinguang Liao,
  • Bin Li,
  • Jiajun Qian,
  • Yong Wu,
  • Xiaoyan Li

摘要

Pulmonary hypertension (PH) is associated with fluid shear stress (FSS) and Gremlin1 (Grem1), but the mechanism by which FSS acts on Grem1 remains unclear. Here we found that FSS downregulated Grem1 in bEnd.3 cells. Meanwhile, FSS inhibited the expression of transcription factor EGR1. Mechanistically, FSS inhibited the transcriptional activity of Grem1 promoter by down-regulating EGR1. RNA-seq and cell function analysis indicated that FSS inhibited the cell cycle and proliferation through the EGR1/Grem1 axis in bEnd.3 cells. In addition, FSS also down-regulated the expression of Grem1 and EGR1 in mouse/rat pulmonary microvascular endothelial cells. Together, our findings revealed the mechanism by which FSS inhibited the cell cycle and proliferation of vascular endothelial cells through the EGR1/Grem1 axis, providing new insights into the development of PH.