ArticlePhysiological research2021
MiR-133a-3p relieves the oxidative stress induced trophoblast cell apoptosis through the BACH1/Nrf2/HO-1 signaling pathway.
Article in Physiological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- The role of miRNA in modulating oxidative stress in preeclampsia: current knowledge.RNA biology · 2026Review
- Elevated BACH1 Contributes to Mitochondrial Succinylome Remodeling and Trophoblast Bioenergetic Dysfunction in Preeclampsia.Antioxidants (Basel, Switzerland) · 2026Article
- Investigating the Regulatory Mechanisms and Prognostic Significance of miR-941 Targeting the Nrf2/Keap1 Pathway in Elderly Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- Circulating miR-145-5p and miR-133a-3p in pediatric sickle cell disease: biomarker potential for vaso-occlusive crises and disease activity.Annals of hematology · 2025Article
- Circulating extracellular vesicles regulate ELAVL1 by delivering miR-133a-3p which affecting NLRP3 mRNA stability inhibiting PANoptosome formation.Biology direct · 2025Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Engineering human bone marrow-derived mesenchymal stromal cell aggregates for enhanced extracellular vesicle secretion in a vertical-wheel bioreactor.Frontiers in bioengineering and biotechnology · 2025Article
- Spatial multiomic landscape of the human placenta at molecular resolution.Nature medicine · 2024Article
- Circulating extracellular vesicular microRNA signatures in early gestation show an association with subsequent clinical features of pre-eclampsia.Scientific reports · 2024Article
- Cardiovascular Disease and miRNAs: Possible Oxidative Stress-Regulating Roles of miRNAs.Antioxidants (Basel, Switzerland) · 2024Review
- MicroRNA-206 Contributes to the Progression of Preeclampsia by Suppressing the Viability and Mobility of Trophocytes via the Inhibition of AGTR1.Physiological research · 2023Article
- Effects of Perilla Seed Meal on Productive Performance, Egg Quality, Antioxidant Capacity and Hepatic Lipid Metabolism of Wenchang Breeder Hens.Animals : an open access journal from MDPI · 2023Article
- Integrated bioinformatic analysis reveals NOS2 as a novel ferroptosis-related biomarker for pre-eclampsia.BMC pregnancy and childbirth · 2023Article
- Hypoxia Inducible Factors (HIF1α and HIF3α) are differentially methylated in preeclampsia placentae and are associated with birth outcomes.Molecular and cellular biochemistry · 2023Article
- Review
- Hydrogen sulfide plays an important role by regulating endoplasmic reticulum stress in myocardial diseases.Frontiers in pharmacology · 2023Review
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- Article
- Effects of Stellera chamaejasme on microvascular density and apoptosis of cancer cells in a rat bladder tumor model.Translational andrology and urology · 2022Article
- [Differential expression profile of miRNAs in amniotic fluid exosomes from fetuses with Down syndrome].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a major cause of the pregnancy morbidity and mortality over the world. Disorganized placentation caused by trophoblast cell abnormity is one of main risk factors to induce PE. MiR-133a-3p has been shown to contain regulatory effects on oxidative stress in the cardiomyocytes. But the effects of miR-133a-3p on oxidative stress-induced apoptosis in the trophoblast cells remain unknown. In this study, trophoblast HTR-8/SVneo cells were transfected with miR-133a-3p mimics and inhibitor. H2O2 (250 microM) treatment of cells was adopted to induce oxidative stress. A series of typical molecular and cellular experiments was subsequently performed in order to investigate this issue. It was found that miR-133a-3p overexpression attenuated the oxidative stress induced by H2O2 through reduced ROS and MDA levels and enhanced antioxidase activities in the trophoblast cells. Overexpressed miR-133a-3p was shown to relieve the oxidative stress-induced apoptosis of HTR-8/SVneo cells. At molecular levels, a direct binding effect of miR-133a-3p on BACH1 was verified. Moreover, miR-133a-3p overexpression also enhanced BACH1 downstream Nrf2/HO-1 signaling to activate antioxidant genes. It is collectively demonstrated that miR-133a-3p can relieve the oxidative stress-induced apoptosis in the trophoblast cells through the BACH1/Nrf2/HO-1 signaling pathway via targeting BACH1 directly. This regulatory mechanism of miR-133a-3p in the trophoblast cells under oxidative stress may give a new perspective for oxidative stress-induced trophoblast cell abnormality and be useful to study more pathological mechanisms of PE.
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