ArticleCell stress & chaperones2012
Increased immunogenicity is an integral part of the heat shock response following renal ischemia.
Article in Cell stress & chaperones, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 10 citations in OpenAlex.
- Bimodal role of NADPH oxidases in the regulation of biglycan-triggered IL-1β synthesis.Matrix biology : journal of the International Society for Matrix Biology · 2016Article
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7 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Renal ischemia increases tubular immunogenicity predisposing to increased risk of kidney allograft rejection. Ischemia-reperfusion not only disrupts cellular homeostasis but also induces the cytoprotective heat shock response that also plays a major role in cellular immune and defense processes. This study therefore tested the hypothesis that upregulation of renal tubular immunogenicity is an integral part of the heat shock response after renal ischemia. Expressions of 70 kDa heat shock protein (Hsp70), major histocompatibility complex (MHC) class II, and intercellular adhesion molecule-1 (ICAM-1) were assessed in normal rat kidney (NRK) cells following ATP depletion (antimycin A for 3 h) and heat (42°C for 24 h). In vitro, transient Hsp70 transfection and heat shock factor-1 (HSF-1) transcription factor decoy treatment were performed. In vivo, ischemic renal cortex was investigated in Sprague-Dawley rats following unilateral renal artery clamping for 45 min and 24 h recovery. Upregulation of Hsp70 was closely and significantly correlated with upregulation of MHC class II and/or ICAM-1 following ATP depletion and heat injury. Bioinformatics analysis searching the TRANSFAC database predicted HSF-1 binding sites in these genes. HSF-1 decoy significantly reduced the expression of immunogenicity markers in stressed NRK cells. In the in vivo rat model of renal ischemia, concordant upregulation of MHC class II molecules and Hsp70 suggests biological relevance of this link. The results demonstrate that upregulation of renal tubular immunogenicity is an integral part of the heat shock response after renal ischemia. Bioinformatic analysis predicted a molecular link to tubular immunogenicity at the level of the transcription factor HSF-1 that was experimentally verified by HSF-1 decoy treatment. Future studies in HSF-1 knockout mice are needed.
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