Open AccessInhibiting USP14 ameliorates inflammatory responses in trophoblast cells by suppressing MAPK/NF‐κB signaling
Author(s) -
Zhao Yingzi,
Zong Fang
Publication year - 2021
Publication title -
immunity, inflammation and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 18
ISSN - 2050-4527
DOI - 10.1002/iid3.465
Subject(s) - proinflammatory cytokine , gene knockdown , downregulation and upregulation , trophoblast , preeclampsia , cytokine , immunology , small interfering rna , biology , nf κb , cancer research , microbiology and biotechnology , medicine , signal transduction , inflammation , fetus , cell culture , rna , placenta , gene , pregnancy , genetics
Abstract Background Preeclampsia can cause severe consequences for pregnant women and infants, and developing effective medicine or methods to prevent or treat patients with preeclampsia is urgently needed. Ubiquitin‐specific protease 14 (USP14) has emerged as a critical regulator in the development of human cancers and neurodegenerative diseases. However, its role in preeclampsia remains elusive. Methods The expression of USP14 in placental tissues from healthy donors and preeclampsia patients were determined by quantitative reverse transcription PCR assay. The protein levels of targeted genes were evaluated by Western blotting assay. Small interfering RNA‐mediated gene knockdown was used to reduce USP14 expression in trophoblast cell lines. Results The expression levels of USP14 and proinflammatory cytokine were substantially upregulated in placental tissues from preeclampsia patients. Knockdown or inhibition of USP14 significantly abrogated hypoxia/reoxygenation‐induced upregulation of nuclear factor kappa B (NF‐κB) activation and proinflammatory cytokine production. Conclusion Our results suggested that USP14 promotes proinflammatory cytokine production through activation of NF‐κB. Developing drugs targeting USP14 may be beneficial for the prevention or treatment of patients with preeclampsia.