title: Kidney function after in vivo gene silencing of uncoupling protein-2 in streptozotocin-induced diabetic rats.
abstract: Kidney uncoupling protein 2 (UCP-2) increases in streptozotocin-induced diabetes, resulting in mitochondria uncoupling, i.e., increased oxygen consumption unrelated to active transport. The present study aimed to investigate the role of UCP-2 for normal and diabetic kidney function utilizing small interference RNA (siRNA) to reduce protein expression. Diabetic animals had increased glomerular filtration rate and kidney oxygen consumption, resulting in decreased oxygen tension and transported sodium per consumed oxygen. UCP-2 protein levels decreased 2 and 50% after UCP-2 siRNA administration in control and diabetic animals respectively. Kidney function was unaffected by in vivo siRNA-mediated gene silencing of UCP-2. The reason for the lack of effect of reducing UCP-2 is presently unknown but may involve compensatory mitochondrial uncoupling by the adenosine nucleotide transporter.
authors.affiliation: Division of Integrative Physiology, Department of Medical Cell Biology, Biomedical Center, Uppsala University, 571, 75123, Uppsala, Sweden. Malou.Friederich@mcb.uu.se.
authors.forename: Malou Friederich
authors.initials: MF
authors.lastname: Persson
authors.affiliation: Division of Nephrology and Hypertension, Department of Medicine, Medical Center, Georgetown University, Washington, DC, USA.
authors.forename: William J
authors.initials: WJ
authors.lastname: Welch
authors.affiliation: Division of Nephrology and Hypertension, Department of Medicine, Medical Center, Georgetown University, Washington, DC, USA.
authors.forename: Christopher S
authors.initials: CS
authors.lastname: Wilcox
authors.affiliation: Division of Integrative Physiology, Department of Medical Cell Biology, Biomedical Center, Uppsala University, 571, 75123, Uppsala, Sweden.|Division of Nephrology and Hypertension, Department of Medicine, Medical Center, Georgetown University, Washington, DC, USA.|Department of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
authors.forename: Fredrik
authors.initials: F
authors.lastname: Palm
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000503:physiopathology*; D020868:Gene Silencing; D005919:Glomerular Filtration Rate; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D007677:Kidney Function Tests; D008297:Male; D008928:Mitochondria / Q000473:pathology*; D024101:Mitochondrial Proteins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D010101:Oxygen Consumption; D034741:RNA, Small Interfering / Q000235:genetics*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000071246:Uncoupling Protein 2
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D034741:RNA, Small Interfering; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2