CLDN3 expression and function in pregnancy‑induced hypertension
- Aixin Zhao
- Yunfang Qi
- Kun Liu
Affiliations: Department of Obstetrics, Laiwu Maternal and Child Health Hospital, Laiwu, Shandong 271199, P.R. China
- Published online on: July 31, 2020 https://doi.org/10.3892/etm.2020.9084
Copyright: © Zhao
et al. This is an open access article distributed under the
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Commons Attribution License.
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This aim of the present study was to investigate the expression and function of claudin 3 (CLDN3) in pregnancy‑induced hypertension. The mRNA expression levels of CLDN3 in the placental tissue and peripheral blood of patients with pregnancy‑induced hypertension were measured using reverse transcription‑quantitative PCR. Human trophoblast HTR8/SVneo cells overexpressing CLDN3 were generated using a lentiviral vector. Cell Counting kit‑8 (CCK‑8) assay, flow cytometry, Transwell chamber assays, confocal laser scanning microscopy and western blot analysis were performed to detect cell proliferation, invasion, migration and apoptosis, in addition to matrix metalloproteinase (MMP) expression and ERK1/2 phosphorylation. The mRNA expression levels of CLDN3 were significantly reduced in the placental tissues and peripheral blood samples of patients with pregnancy‑induced hypertension compared with healthy pregnant controls. CLDN3 overexpression significantly increased HTR8/SVneo cell proliferation, invasion and migration whilst reducing apoptosis. HTR8/SVneo cells overexpressing CLDN3 also exhibited increased myofiber levels, increased MMP‑2 and MMP‑9 expression and increased ERK1/2 signaling activity. CLDN3 downregulation may be associated with the pathogenesis of pregnancy‑induced hypertension. In conclusion, CLDN3 promotes the proliferative and invasive capabilities of human trophoblast cells, with the underlying mechanisms possibly involving upregulation of MMP expression via the ERK1/2 signaling pathway.