ArticleBMC molecular and cell biology2019
Protective effect of silencing Stat1 on high glucose-induced podocytes injury via Forkhead transcription factor O1-regulated the oxidative stress response.
Article in BMC molecular and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- The PRMT6/STAT1/ACSL1 axis promotes ferroptosis in diabetic nephropathy.Cell death and differentiation · 2024Article
- Effect of Nicotine on STAT1 Pathway and Oxidative Stress in Rat Lungs.Reports of biochemistry & molecular biology · 2021Article
- Pharmacological Actions, Molecular Mechanisms, Pharmacokinetic Progressions, and Clinical Applications of Hydroxysafflor Yellow A in Antidiabetic Research.Journal of immunology research · 2021Review
- Forsythoside A Alleviates High Glucose-Induced Oxidative Stress and Inflammation in Podocytes by Inactivating MAPK Signaling via MMP12 Inhibition.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Renoprotective effect ofAmerican journal of physiology. Renal physiology · 2021Article
- Restraint Stress Alters Expression of Glucocorticoid Bioavailability Mediators, Suppresses Nrf2, and Promotes Oxidative Stress in Liver Tissue.Antioxidants (Basel, Switzerland) · 2020Article
- FoxO1-mediated inhibition of STAT1 alleviates tubulointerstitial fibrosis and tubule apoptosis in diabetic kidney disease.EBioMedicine · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundPodocyte plays an important role in maintaining the integrity and function of the glomerular filtration barrier. Various studies reported that forkhead transcription factor (Fox) O1 played a key role in anti-oxidative signaling. This study aimed to investigate the role of Stat1 in high glucose (HG) -induced podocyte injury.
methodsUnder normal glucose, hypertonic and HG stimulated podocyte conditions, cell counting kit-8 (CCK-8) assay, flow cytometry and western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were respectively carried out to determine cell viability, apoptosis, reactive oxygen species (ROS) production and related genes expressions. We then respectively used silent Stat1, simultaneous silencing Stat1 and FoxO1 and over-expression of FoxO1, to observe whether they/it could reverse the damage of podocytes induced by HG.
resultsHigh glucose attenuated cell survival and promoted cell apoptosis in MPC-5 cells at the same time, and it was also observed to promote the protein expression of Stat1 and the FoxO1 expression inhibition. Silencing Stat1 could reverse HG-induced podocytes injury. Specifically, siStat1 increased cell viability, inhibited cell apoptosis and attenuated ROS level in a high-glucose environment. Cleaved caspase-3 and pro-apoptosis protein Bax was significantly down-regulated, and anti-apoptosis protein Bcl-2 was up-regulated by siStat1. The antioxidant genes Catalase, MnSOD, NQO1 and HO1 were up-regulated by siStat1. We found that silencing FoxO1 reversed the protective effect of siStat1 on the HG-induced podocytes injury.
conclusionsSilencing Stat1 could reverse the effects of high glucose-triggered low cell viability, cell apoptosis and ROS release and the functions of Stat1 might be involved in FoxO1 mediated-oxidative stress in nucleus.
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