ArticleBMC pregnancy and childbirth2023
High TXNIP expression accelerates the migration and invasion of the GDM placenta trophoblast.
Article in BMC pregnancy and childbirth, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 12 citations in OpenAlex.
- Ferroptosis-Mediated Placental Dysfunction in the Pathophysiology of Gestational Diabetes Mellitus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- TP53BP2 Promotes Placental Autophagy and Preeclampsia via G9a and DNMT1 Cooperatively Modulating E2F1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unraveling the complex web: pathogenesis and prevention of gestational diabetes mellitus-related fetal overgrowth.Frontiers in cell and developmental biology · 2026Review
- Oxidative stress, mitochondrial dysfunction, and ferroptosis in the placenta of gestational diabetes mellitus.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Enhanced SLC2A4 expression mitigates insulin resistance in gestational diabetes mellitus via the FoxO signaling pathwayExperimental and therapeutic medicine · 2025Article
- HOXA13 promotes high glucose-induced trophoblast cell growth and migration during gestational diabetes by regulating the smad2 pathway.Hereditas · 2025Article
- Review
- Association between cardiometabolic index and gestational diabetes mellitus: a cross-sectional study.Endocrine · 2025Article
- Transcriptome Sequencing Identifies PCK1 and IRS4 as Key Regulators of Gestational Diabetes Mellitus in Placenta: A Pilot Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Elevated TXNIP and reduced PINK1 in gestational diabetes mellitus: association with dyslipidemia and pregnancy complications.American journal of translational research · 2025Article
- Placental Bioenergetics and Antioxidant Homeostasis in Maternal Obesity and Gestational Diabetes.Antioxidants (Basel, Switzerland) · 2024Article
- Unraveling the molecular mechanisms driving enhanced invasion capability of extravillous trophoblast cells: a comprehensive review.Journal of assisted reproduction and genetics · 2024Review
- A Critical Review on Varied Aspects of Gestational Diabetes Mellitus (GDM) and It's Associations with Placenta.Indian journal of endocrinology and metabolismReview
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14 authors at 5 institutions in 1 country.
Funding
Abstract
introductionOur previous study has proofed the glucose sensitive gene-thioredoxin-interacting protein (TXNIP) expression was up in the placenta of the patients with gestational diabetes mellitus (GDM), but the pathological mechanisms underlying abnormal TXNIP expression in the placenta of patients with GDM is completely unclear and additional investigations are required to explain the findings we have observed. In the present study, we simulated the high TXNIP expression via introducing the Tet-On "switch" in vitro, approximate to its expression level in the real world, to explore the following consequence of the abnormal TXNIP.
methodsThe expression and localization of TXNIP in the placenta of GDM patients and the health control was investigated via immunofluorescent staining, western blot and RT-qPCR. Overexpression of TXNIP was achieved through transfecting Tet-on system to the human trophoblastic cell line-HTR-8/Svneo cell. TXNIP knockout was obtained via CRISPR-Cas9 method. The cell phenotype was observed via IncuCyte Imaging System and flow cytometry. The mechanism was explored via western blot and RT-qPCR.
resultsThe expression level of TXNIP in the GDM placenta was nearly 2-3 times higher than that in the control. The TXNIP located at trophoblastic cells of the placenta. When the expression of TXNIP was upregulated, the migration and invasion of the cells accelerated, but cell apoptosis and proliferation did not changed compared with the control group. Furthermore, the size of the TetTXNIP cells became larger, and the expression level of Vimentin and p-STAT3 increased in the TetTXNIP cells. All the changes mentioned above were opposite in the TXNIP-KO cells.
conclusionsAbnormal expression of TXNIP might be related to the impairment of the GDM placental function, affecting the migration and invasion of the placental trophoblast cells through STAT3 and Vimentin related pathway; thus, TXNIP might be the potential therapeutic target for repairing the placental dysfunction deficient in GDM patients.
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