CALL FOR PAPERS Pathophysiology of Acute Kidney Injury Reactive oxygen species and IRF1 stimulate IFN production by proximal tubules during ischemic AKI
نویسندگان
چکیده
Pamela D. Winterberg, Yanxia Wang, Keng-Mean Lin, John R. Hartono, Glenn T. Nagami, Xin J. Zhou, John M. Shelton, James A. Richardson, and Christopher Y. Lu Department of Pediatrics, Nephrology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Internal Medicine, Nephrology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Internal Medicine, Cardiology Division, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas; Graduate School of Biomedical Sciences (Immunology), University of Texas Southwestern Medical Center, Dallas, Texas; and Nephrology Section, Veterans Affairs Greater Los Angeles and University of California, Los Angeles, California
منابع مشابه
Reactive oxygen species and IRF1 stimulate IFNα production by proximal tubules during ischemic AKI.
We previously reported that expression of the transcription factor interferon regulatory factor 1 (IRF1) is an early, critical maladaptive signal expressed by renal tubules during murine ischemic acute kidney injury (AKI). We now show that IRF1 mediates signals from reactive oxygen species (ROS) generated during ischemic AKI and that these signals ultimately result in production of α-subtypes o...
متن کاملReactive oxygen species ( ROS ) and IRF 1 stimulate IFN α production by 1 proximal tubules during ischemic AKI
Reactive oxygen species (ROS) and IRF1 stimulate IFNα production by 1 proximal tubules during ischemic AKI. 2 Pamela D. Winterberg, Yanxia Wang, Keng-Mean Lin, John R. Hartono, Glenn T. Nagami, Xin J. Zhou, 3 John M. Shelton, James A. Richardson, and Christopher Y. Lu . 4 5 Author Contributions: PDW and YW contributed equally to the majority of experimental data presented; PDW 6 participated in...
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Acute renal ischemia elicits an inflammatory response that may exacerbate acute kidney injury, but the regulation of the initial signals that recruit leukocytes is not well understood. Here, we found that IFN regulatory factor 1 (IRF-1) was a critical, early proinflammatory signal released during ischemic injury in vitro and in vivo. Within 15 min of reperfusion, proximal tubular cells of the S...
متن کاملp66SHC-mediated mitochondrial dysfunction in renal proximal tubule cells during oxidative injury.
Mitochondrial dysfunction is involved in pathopysiology of ischemia-reperfusion-induced acute kidney injury (AKI). The p66shc adaptor protein is a newly recognized mediator of mitochondrial dysfunction, which might play a role in AKI-induced renal tubular injury. Oxidative stress-mediated Serine36 phosphorylation of p66shc facilitates its transportation to the mitochondria where it oxidizes cyt...
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BACKGROUND Chronic nicotine (Ch-NIC) exposure exacerbates ischemia/reperfusion (I/R)-induced oxidative stress and acute kidney injury (AKI), and mitochondrial production of reactive oxygen species (ROS) in cultured renal proximal tubule cells (RPTCs). Because Ser36-phosphorylated p66shc modulates mitochondrial ROS production and injury of RPTCs, we hypothesized that Ch-NIC exacerbates AKI by in...
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