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CLDN3 expression and function in pregnancy-induced hypertension
Aixin Zhao1, Yunfang Qi1, Kun Liu1
1Department of Obstetrics, Laiwu Maternal and Child Health Hospital, Laiwu, Shandong 271199, P.R. China.
Experimental and Therapeutic Medicine
|August 29, 2020
Summary
Claudin 3 (CLDN3) is reduced in pregnancy-induced hypertension. CLDN3 enhances trophoblast cell proliferation and invasion, potentially via the ERK1/2 pathway, suggesting a role in disease pathogenesis.
Area of Science:
- Obstetrics and Gynecology
- Molecular Biology
- Cell Biology
Background:
- Pregnancy-induced hypertension (PIH) is a significant complication of pregnancy.
- The role of tight junction proteins, such as claudin 3 (CLDN3), in PIH pathogenesis is not well understood.
Purpose of the Study:
- To investigate the expression and function of CLDN3 in PIH.
- To elucidate the molecular mechanisms underlying CLDN3's role in trophoblast cell behavior.
Main Methods:
- Quantitative reverse transcription PCR (RT-qPCR) to measure CLDN3 mRNA levels in placental tissue and blood.
- Generation of CLDN3-overexpressing human trophoblast cells (HTR8/SVneo) using lentiviral vectors.
- Assays for cell proliferation (CCK-8), apoptosis (flow cytometry), invasion, and migration (Transwell), alongside Western blot for MMPs and ERK1/2 phosphorylation.
Main Results:
- CLDN3 mRNA expression was significantly decreased in placental tissues and peripheral blood of PIH patients compared to healthy controls.
- CLDN3 overexpression in HTR8/SVneo cells enhanced proliferation, invasion, and migration while reducing apoptosis.
- Overexpression of CLDN3 led to increased matrix metalloproteinase (MMP-2, MMP-9) expression and elevated ERK1/2 signaling.
Conclusions:
- CLDN3 downregulation is potentially associated with the pathogenesis of PIH.
- CLDN3 promotes human trophoblast cell proliferation and invasion, possibly by upregulating MMP expression through the ERK1/2 signaling pathway.
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