Ubiquitin-Specific Peptidase 5 is Involved in the Proliferation of Trophoblast Cells by Regulating Wnt/β-Catenin Signaling

• Published in: Molecular biotechnology 2021-08, Vol.63 (8), p.686-693
• Main Authors: Li, Liu, Wang, Shuo, Wang, Ming, Qi, Guoqing, Zhao, Hongliang
• Format: Article
• Language: English
• Subjects: Antibodies; beta Catenin - metabolism; Biochemistry; Biological Techniques; Biotechnology; c-Myc protein; Cancer; Cardiology; Cell Biology; Cell Proliferation; Cell Survival; Cell viability; Cells, Cultured; Chemistry; Chemistry and Materials Science; Cholecystokinin; Cyclin D1; Endopeptidases - genetics; Endopeptidases - metabolism; Female; Gene Expression Regulation; Human Genetics; Humans; Hypoxia; Medical research; Myc protein; Original Paper; Peptidase; Peptidases; Placenta; Placenta - metabolism; Placenta - pathology; Plasmids; Pre-eclampsia; Pre-Eclampsia - metabolism; Pre-Eclampsia - pathology; Preeclampsia; Pregnancy; Protein Science; Proteins; Reperfusion - adverse effects; Signal transduction; Signaling; Silence; Trophoblasts - enzymology; Trophoblasts - metabolism; Trophoblasts - pathology; Ubiquitin; Wnt protein; Wnt Signaling Pathway - genetics; Womens health; β-Catenin
• ISSN: 1073-6085; 1559-0305
• DOI: 10.1007/s12033-021-00330-x

Preeclampsia (PE) is a pathologic condition in pregnant women which accounts for the inhibition of proliferation, migration and invasion of trophoblast cells. This study aimed to investigate the regulation of ubiquitin-specific peptidase 5 (USP5) on the trophoblast cells in PE. Expressions of USP5 in the placentas of PE patients and healthy donors were examined by qRT-PCR and Western blot. Hypoxia/reoxygenation (H/R) model in trophoblast cells was further established. Cell viability was examined using CCK-8 assay. Finally, the effect of overexpression and silence of USP5 using lentivirus transduction was studied. Our results showed that USP5 was lowly expressed in the placentas of PE patients as well as in H/R-induced trophoblast cells. In the experiments of overexpression, USP5 promoted the proliferation of trophoblast cells, and up-regulated the expressions of β-catenin and the downstream signals c-Myc and Cyclin D1 in trophoblast cells. On the other hand, silence of USP5 elicited the opposite results. The overexpression of USP5 in the H/R model greatly released the H/R-induced inhibition in the trophoblast cells, and moderated the down-regulation of β-catenin and c-Myc induced by H/R. We concluded that USP5 promoted the proliferation of trophoblast cells via the up-regulation of the Wnt/β-catenin signaling pathway.