Activation of the epithelial sodium channel (ENaC) leads to cytokine profile shift to pro-inflammatory in labor

Xiao Sun, Jing Hui Guo, Dan Zhang, Jun jiang Chen, Wei Yin Lin, Yun Huang, Hui Chen, Wen Qing Huang, Yifeng Liu, Lai Ling Tsang, Mei Kuen Yu, Yiu Wa Chung, Xiaohua Jiang, Hefeng Huang, Hsiao Chang Chan, Ye Chun Ruan

Research output: Journal article publicationJournal articleAcademic researchpeer-review

6 Citations (Scopus)


The shift of cytokine profile from anti- to pro-inflammatory is the most recognizable sign of labor, although the underlying mechanism remains elusive. Here, we report that the epithelial sodium channel (ENaC) is upregulated and activated in the uterus at labor in mice. Mechanical activation of ENaC results in phosphorylation of CREB and upregulation of pro-inflammatory cytokines as well as COX-2/PGE2 in uterine epithelial cells. ENaC expression is also upregulated in mice with RU486-induced preterm labor as well as in women with preterm labor. Interference with ENaC attenuates mechanically stimulated uterine contractions and significantly delays the RU486-induced preterm labor in mice. Analysis of a human transcriptome database for maternal–fetus tissue/blood collected at onset of human term and preterm births reveals significant and positive correlation of ENaC with labor-associated pro-inflammatory factors in labored birth groups (both term and preterm), but not in non-labored birth groups. Taken together, the present finding reveals a pro-inflammatory role of ENaC in labor at term and preterm, suggesting it as a potential target for the prevention and treatment of preterm labor.

Original languageEnglish
Article numbere8868
JournalEMBO Molecular Medicine
Issue number10
Publication statusPublished - Oct 2018


  • ENaC
  • labor/parturition
  • preterm labor
  • pro-inflammatory

ASJC Scopus subject areas

  • Molecular Medicine


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