ArticleThe Journal of urology2008
Tumor necrosis factor-alpha induces intrinsic apoptotic signaling during renal obstruction through truncated bid activation.
Article in The Journal of urology, 2008. 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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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
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- TNF-α-Mediated Endothelial Cell Apoptosis Is Rescued by Hydrogen Sulfide.Antioxidants (Basel, Switzerland) · 2023Article
- Anti-Apoptotic Effect of G-Protein-Coupled Receptor 40 Activation on Tumor Necrosis Factor-α-Induced Injury of Rat Proximal Tubular Cells.International journal of molecular sciences · 2019Article
- Electroacupuncture Reduced Apoptosis of Hippocampal Neurons in Mice with Cerebral Infarction by Regulating the Notch3 Signaling Pathway.Journal of molecular neuroscience : MN · 2019Article
- Melittin Inducing the Apoptosis of Renal Tubule Epithelial Cells through Upregulation of Bax/Bcl-2 Expression and Activation of TNF-BioMed research international · 2019Article
- Tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability: role of intrinsic apoptotic signaling.Journal of physiology and biochemistry · 2014Article
- The role of intrinsic apoptotic signaling in hemorrhagic shock-induced microvascular endothelial cell barrier dysfunction.Journal of cardiovascular translational research · 2014Review
- Regulation of tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability by recombinant B-cell lymphoma-extra large.The Journal of surgical research · 2013Article
- Anti-apoptotic effect of claudin-1 on TNF-α-induced apoptosis in human breast cancer MCF-7 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Ischemic kidney injury and mechanisms of tissue repair.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
purposeTumor necrosis factor-alpha has a significant role in renal tubular cell apoptosis during obstruction induced renal injury. While we have previously reported the role of tumor necrosis factor-alpha in extrinsic pathway apoptotic signaling during renal obstruction, to our knowledge its effect on intrinsic pathway signaling and mitochondrial release of cytochrome C has not previously been evaluated. MATERIALS AND
methodsMale Sprague-Dawley rats were anesthetized and underwent unilateral ureteral obstruction vs sham operation. At 24 hours before surgery and every 84 hours thereafter the animals received vehicle or a pegylated form of soluble tumor necrosis factor receptor type 1. The kidneys were harvested 1 week postoperatively. The renal cortex was analyzed for tumor necrosis factor-alpha production (enzyme-linked immunosorbent assay), apoptosis (TUNEL and enzyme-linked immunosorbent assay), Bcl-2, Bcl-x(L), Bax, caspase 8 and truncated Bid expression (Western blot), and mitochondrial cytochrome C release (immunohistochemistry).
resultsRenal obstruction induced increased tumor necrosis factor-alpha production, apoptotic renal tubular death, the expression of Bax, caspase 8 and truncated BID, and mitochondrial release of cytochrome C, while simultaneously stimulating decreased Bcl-2 and Bcl-x(L) expression. Treatment with the pegylated form of soluble tumor necrosis factor receptor type 1 significantly decreased obstruction induced tumor necrosis factor-alpha production, apoptosis, Bax, caspase 8, truncated Bid expression and mitochondrial cytochrome C release, and increased Bcl-2 and Bcl-x(L) expression.
conclusionsThese results demonstrate that tumor necrosis factor-alpha stimulates Bid and subsequent intrinsic apoptotic signaling pathway activation during unilateral ureteral obstruction, resulting in mitochondrial cytochrome C release and apoptotic cell death. We identified tumor necrosis factor-alpha neutralization as a potential therapeutic option for ameliorating obstruction induced renal injury.
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