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Objective <p>Disruptions to trophoblast infiltration and placental implantation are recognized as pivotal early mechanisms underlying the pathogenesis of preeclampsia. Previous studies have reported the aberrant expression of PTPRN2 in preeclamptic placentas, yet its precise pathological role remains poorly defined. The present study investigated the functional involvement of PTPRN2 in regulating trophoblast invasion.</p> Methods <p>PTPRN2 expression was detected by qRT-PCR and Western blotting in normal and preeclamptic placentas, as well as in HTR-8/SVneo cells cultured under normoxic or hypoxic conditions. HTR-8/SVneo cells were then transfected with a PTPRN2 overexpression plasmid. Transwell assays were performed to evaluate trophoblast invasion ability. Additionally, the expression of key Wnt/β-catenin signaling components, including β-catenin and GSK-3β was analyzed in PTPRN2-overexpressing HTR-8/SVneo cells and preeclamptic placentas.</p> Results <p>Our results demonstrated that PTPRN2 was significantly upregulated in preeclamptic placental tissues. In vitro experiments further revealed that hypoxic exposure induced PTPRN2 expression in HTR-8/SVneo cells and that overexpression of PTPRN2 markedly suppressed the invasive ability of these cells. Moreover, hypoxia decreased the protein levels of β‑catenin and GSK‑3β in HTR-8/SVneo cells, and these effects were further exacerbated by PTPRN2 overexpression.</p> Conclusion <p>Collectively, these findings indicate that hypoxia‑induced upregulation of PTPRN2 contributes to impaired trophoblast invasion via inhibition of the Wnt/β‑catenin signaling pathway.</p>

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Hypoxia-Induced PTPRN2 Suppresses Trophoblast Invasion via Wnt/β-Catenin Pathway Inhibition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月19日

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  • Tong Zhu,
  • Wan-jiang Zeng,
  • Ying Zhang

摘要

Objective

Disruptions to trophoblast infiltration and placental implantation are recognized as pivotal early mechanisms underlying the pathogenesis of preeclampsia. Previous studies have reported the aberrant expression of PTPRN2 in preeclamptic placentas, yet its precise pathological role remains poorly defined. The present study investigated the functional involvement of PTPRN2 in regulating trophoblast invasion.

Methods

PTPRN2 expression was detected by qRT-PCR and Western blotting in normal and preeclamptic placentas, as well as in HTR-8/SVneo cells cultured under normoxic or hypoxic conditions. HTR-8/SVneo cells were then transfected with a PTPRN2 overexpression plasmid. Transwell assays were performed to evaluate trophoblast invasion ability. Additionally, the expression of key Wnt/β-catenin signaling components, including β-catenin and GSK-3β was analyzed in PTPRN2-overexpressing HTR-8/SVneo cells and preeclamptic placentas.

Results

Our results demonstrated that PTPRN2 was significantly upregulated in preeclamptic placental tissues. In vitro experiments further revealed that hypoxic exposure induced PTPRN2 expression in HTR-8/SVneo cells and that overexpression of PTPRN2 markedly suppressed the invasive ability of these cells. Moreover, hypoxia decreased the protein levels of β‑catenin and GSK‑3β in HTR-8/SVneo cells, and these effects were further exacerbated by PTPRN2 overexpression.

Conclusion

Collectively, these findings indicate that hypoxia‑induced upregulation of PTPRN2 contributes to impaired trophoblast invasion via inhibition of the Wnt/β‑catenin signaling pathway.