ArticleJournal of molecular histology2021
MiR-133b regulates oxidative stress injury of trophoblasts in preeclampsia by mediating the JAK2/STAT3 signaling pathway.
Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Changes in microRNA expression associated with preeclampsia: a systematic review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Pooled it
- The role of miRNA in modulating oxidative stress in preeclampsia: current knowledge.RNA biology · 2026Review
- Review
- Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025Review
- Non-coding RNAs: the architects of placental development and pregnancy success.Molecular genetics and genomics : MGG · 2025Review
- HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction.Experimental and therapeutic medicine · 2024Article
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a pregnancy-related syndrome. Aberrant placental microRNAs (miRNAs) expression might associate with PE, including miR-133b. However, its role in the pathogenesis of preeclampsia remains elusive. Therefore, this study explored the role of miR-133b in oxidative stress injury of trophoblasts in preeclampsia (PE) by mediating the JAK2/STAT3 signaling pathway. Placental tissues were collected from PE patients to detect the expression of miR-133b and JAK2/STAT3. Then, in vitro experiments were performed on human extravillous trophoblast-derived HTR-8/SVneo cells, which were divided into Normal, hypoxia/reoxygenation (H/R), H/R + miR-NC, H/R + miR-133b inhibitor, H/R + JAK2 siRNA and H/R + miR-133b inhibitor + JAK2 siRNA groups. Cell invasion and migration abilities were detected by Transwell and wound healing assays, while apoptosis was detected by flow cytometry. The intracellular oxidative stress levels were also measured. Furthermore, the expression of miR-133b and the JAK2/STAT3 pathway was determined by qRT-PCR and Western blotting. We found that miR-133b was up-regulated, with decreases in JAK2 and p-STAT3/STAT3 in placental tissues of PE patients. Additionally, HTR8/SVneo cells in the H/R group had decreased invasion and migration abilities with increased apoptotic rates and oxidative stress levels. Moreover, the expression of miR-133b was up-regulated with decreases in p-JAK2 and p-STAT3 in H/R-treated HTR8/SVneo cells. These indicators in the H/R + miR-133b inhibitor group were ameliorated in comparison with those in the H/R group but deteriorated in the H/R + JAK2 siRNA group. Moreover, JAK2 siRNA reversed the positive effect of the miR-133b inhibitor on the invasion and migration abilities of trophoblasts. In summary, inhibiting miR-133b may improve oxidative stress injury to promote the migration and invasion of trophoblasts and suppress apoptosis by activating the JAK2/STAT3 pathway.
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