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Abnormal elevated PANX1 expression hampers endometrial decidualization by upregulating extracellular ATP

Xia-Lu Liu1,2, Qi Yang3, Pei-Pei Liu1,4

  • 1Reproductive Medicine Center, Jiangxi Maternal and Child Health Hospital, Nanchang, Jiangxi Province, People's Republic of China.

Scientific Reports
|March 3, 2026
PubMed

Insights

Abnormal Pannexin1 (PANX1) expression disrupts endometrial decidualization by altering extracellular ATP levels, leading to recurrent implantation failure (RIF). Normal PANX1 levels are crucial for successful embryo implantation.

Area of Science:

  • Reproductive Biology
  • Cellular Mechanisms
  • Molecular Endocrinology

Background:

  • Recurrent implantation failure (RIF) is a major challenge in assisted reproductive technologies, often linked to abnormal endometrial decidualization.
  • The precise molecular mechanisms underlying RIF and decidualization defects remain unclear.
  • Pannexin1 (PANX1), an ATP-permeable channel, influences extracellular ATP (eATP) levels, which are known to affect endometrial decidualization.

Purpose of the Study:

  • To investigate the role of PANX1 in the molecular mechanisms of RIF.
  • To explore the regulatory function of PANX1 on human endometrial stromal cell (HESC) decidualization.
  • To determine if abnormal PANX1 expression contributes to RIF by affecting endometrial receptivity.

Main Methods:

  • Comparative analysis of PANX1 expression in endometrial tissues from RIF patients and controls.
  • In vitro studies using HESCs involving immunofluorescence, Western blot, RT-PCR, plasmid transfection, and ATP detection.
  • Establishment of an animal model to validate in vitro findings.

Main Results:

  • PANX1 expression was significantly upregulated in the endometrial tissue of RIF patients.
  • Overexpression of PANX1 in HESCs led to increased eATP and inhibited decidualization, evidenced by decreased prolactin (PRL) and insulin-like growth factor binding protein 1 (IGFBP-1) expression.
  • Knockdown of PANX1 also impaired HESC decidualization, highlighting the necessity of normal PANX1 levels.
  • Animal models corroborated the in vitro findings.

Conclusions:

  • Abnormal upregulation of PANX1 hinders endometrial decidualization by increasing eATP concentrations, contributing to RIF.
  • This study identifies a novel molecular mechanism contributing to RIF.
  • PANX1 represents a potential therapeutic target for improving embryo implantation rates in RIF patients.
Keywords:
EATPEndometrial decidualizationHuman endometrial stromal cellsPANX1RIF

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