ArticleAmerican journal of physiology. Renal physiology2009
Transglutaminase-1 protects renal epithelial cells from hydrogen peroxide-induced apoptosis through activation of STAT3 and AKT signaling pathways.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Transglutaminase 1: Emerging Functions beyond Skin.International journal of molecular sciences · 2024Review
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- Pharmacological effects of natural medicine ginsenosides against Alzheimer's disease.Frontiers in pharmacology · 2022Review
- JAK2 deficiency improves erectile function in diabetic mice through attenuation of oxidative stress, apoptosis, and fibrosis.Andrology · 2021Article
- Development and Validation of Conditions for Extracting Flavonoids Content and Evaluation of Antioxidant and Cytoprotective Activities fromAntioxidants (Basel, Switzerland) · 2019Article
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- Isozyme-specific comprehensive characterization of transglutaminase-crosslinked substrates in kidney fibrosis.Scientific reports · 2018Article
- Ginsenoside Rg1 Decreases Oxidative Stress and Down-Regulates Akt/mTOR Signalling to Attenuate Cognitive Impairment in Mice and Senescence of Neural Stem Cells Induced by D-Galactose.Neurochemical research · 2018Article
- Article
- Class I HDAC activity is required for renal protection and regeneration after acute kidney injury.American journal of physiology. Renal physiology · 2014Article
- IL-22 ameliorates renal ischemia-reperfusion injury by targeting proximal tubule epithelium.Journal of the American Society of Nephrology : JASN · 2014Article
- JAK2/STAT3 inhibition attenuates noise-induced hearing loss.PloS one · 2014Article
- New role of JAK2/STAT3 signaling in endothelial cell oxidative stress injury and protective effect of melatonin.PloS one · 2013Article
- Beta-actin is a target for transglutaminase activity at synaptic endings in chicken telencephalic cell cultures.Journal of molecular neuroscience : MN · 2012Article
- PrLZ protects prostate cancer cells from apoptosis induced by androgen deprivation via the activation of Stat3/Bcl-2 pathway.Cancer research · 2011Article
- E-cadherin and transglutaminase-1 epithelial barrier restoration precedes type IV collagen basement membrane reconstruction following vocal fold mucosal injury.Cells, tissues, organs · 2011Article
- HIV-1 inhibits autophagy in bystander macrophage/monocytic cells through Src-Akt and STAT3.PloS one · 2010Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Our recent studies showed that transglutaminase-1 (TGase-1) is uniquely expressed in mouse renal proximal tubular cells (RPTC) and mediates cell proliferation. In this study, we investigated the role of TGase-1 in cell survival and the survival signaling pathways regulated by TGase-1 in RPTC following oxidant injury. Exposure of RPTC to hydrogen peroxide (H2O2) resulted in apoptosis and an increase in TGase activity. Inhibition of TGase activity with monodansylcadervine (MDC), a TGase inhibitor, or knockdown of TGase-1 with small interference (si)RNA enhanced apoptosis and decreased cell survival in H2O2-treated RPTC. Conversely, overexpression of TGase-1 rendered RPTC more resistant to H2O2 toxicity and MDC treatment blocked this response. Concurrent with RPTC apoptosis, phosphorylation of AKT, signal transducer and activator of transcription-3 (STAT3), and glucogen synthase kinase-3beta (GSK-3beta) were observed. Pretreatment of cells with MDC or TGase-1 siRNA inhibited phosphorylation of all these molecules. Inhibition of either the AKT or STAT3 pathway potentiated H2O2-induced cell death and increased GSK-3beta activity by dephosphorylation at serine 9. Furthermore, treatment with GSK-3beta inhibitors reduced H2O2-induced apoptosis and abolished the death-promoting effect of AKT and STAT3 inhibition. Therefore, we have identified TGase-1 as a novel survival factor in renal epithelial cells and it contributes to cell survival through activation of the AKT and STAT3 signaling pathways following oxidant injury.
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