Friederich-Persson 2014 Adv Exp Med Biol: Difference between revisions
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{{Publication | {{Publication | ||
|title=Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L ( | |title=Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L (2014) Angiotensin II reduces transport-dependent oxygen consumption but increases transport-independent oxygen consumption in immortalized mouse proximal tubular cells. Adv Exp Med Biol 812:157-63. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/24729228 PMID:24729228] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/24729228 PMID: 24729228] | ||
|authors=Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L | |authors=Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L | ||
|year= | |year=2014 | ||
|journal=Adv Exp Med Biol | |journal=Adv Exp Med Biol | ||
|abstract=Oxidative stress is closely associated with renal dysfunction following diabetes and hypertension. Angiotensin II (Ang II) can activate the NADPH-oxidase, increasing oxidative stress that is thought to blunt proximal tubular electrolyte transport and thereby oxygen consumption (QOโ). We investigated the effect of Ang II on QOโ in immortalized mouse proximal tubular cells over-expressing the NADPH oxidase subunit p22(phox); a model of increased oxidative stress. Cultured cells were exposed to either Ang II or HโOโ for 48 h. QOโ was determined during baseline (113 mmol/l NaCl; transport-dependent QOโ) and during sodium-free conditions (transport-independent QOโ). Ang II reduced transport-dependent QOโ in wild-types, but not in p22(phox) which also displayed increased QOโ at baseline. Transport-independent QOโ was increased in p22(phox) and Ang II had no additional effect, whereas it increased QOโ in wild-type. Addition of HโOโ reduced transport-dependent QOโ in wild-types, but not in p22(phox). Transport-independent QOโ was unaffected by HโOโ. The similar effects of Ang II and HโOโ to reduce transport-dependent QOโ suggest a direct regulatory role of oxidative stress. In accordance, the transport-dependent QOโ was reduced in p22(phox) already during baseline. The effects of Ang II on transport-independent QOโ was not replicated by HโOโ, indicating direct regulation via Ang II-receptors independently of oxidative stress. However, the Ang II effect was absent in p22(phox), suggesting that oxidative stress also modulates normal Ang II signaling. In conclusion, Ang II affects both transport-dependent and transport-independent QOโ in proximal tubular cells and may be an important pathway modulating renal QOโ. | |abstract=Oxidative stress is closely associated with renal dysfunction following diabetes and hypertension. Angiotensin II (Ang II) can activate the NADPH-oxidase, increasing oxidative stress that is thought to blunt proximal tubular electrolyte transport and thereby oxygen consumption (QOโ). We investigated the effect of Ang II on QOโ in immortalized mouse proximal tubular cells over-expressing the NADPH oxidase subunit p22(phox); a model of increased oxidative stress. Cultured cells were exposed to either Ang II or HโOโ for 48 h. QOโ was determined during baseline (113 mmol/l NaCl; transport-dependent QOโ) and during sodium-free conditions (transport-independent QOโ). Ang II reduced transport-dependent QOโ in wild-types, but not in p22(phox) which also displayed increased QOโ at baseline. Transport-independent QOโ was increased in p22(phox) and Ang II had no additional effect, whereas it increased QOโ in wild-type. Addition of HโOโ reduced transport-dependent QOโ in wild-types, but not in p22(phox). Transport-independent QOโ was unaffected by HโOโ. The similar effects of Ang II and HโOโ to reduce transport-dependent QOโ suggest a direct regulatory role of oxidative stress. In accordance, the transport-dependent QOโ was reduced in p22(phox) already during baseline. The effects of Ang II on transport-independent QOโ was not replicated by HโOโ, indicating direct regulation via Ang II-receptors independently of oxidative stress. However, the Ang II effect was absent in p22(phox), suggesting that oxidative stress also modulates normal Ang II signaling. In conclusion, Ang II affects both transport-dependent and transport-independent QOโ in proximal tubular cells and may be an important pathway modulating renal QOโ. | ||
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{{Labeling | {{Labeling | ||
|area=Respiration, Genetic knockout;overexpression | |||
|injuries=Oxidative stress;RONS | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Kidney | |tissues=Kidney, Other cell lines | ||
|instruments=Oxygraph-2k | |||
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|additional= | |||
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Latest revision as of 10:40, 9 November 2016
Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L (2014) Angiotensin II reduces transport-dependent oxygen consumption but increases transport-independent oxygen consumption in immortalized mouse proximal tubular cells. Adv Exp Med Biol 812:157-63. |
Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L (2014) Adv Exp Med Biol
Abstract: Oxidative stress is closely associated with renal dysfunction following diabetes and hypertension. Angiotensin II (Ang II) can activate the NADPH-oxidase, increasing oxidative stress that is thought to blunt proximal tubular electrolyte transport and thereby oxygen consumption (QOโ). We investigated the effect of Ang II on QOโ in immortalized mouse proximal tubular cells over-expressing the NADPH oxidase subunit p22(phox); a model of increased oxidative stress. Cultured cells were exposed to either Ang II or HโOโ for 48 h. QOโ was determined during baseline (113 mmol/l NaCl; transport-dependent QOโ) and during sodium-free conditions (transport-independent QOโ). Ang II reduced transport-dependent QOโ in wild-types, but not in p22(phox) which also displayed increased QOโ at baseline. Transport-independent QOโ was increased in p22(phox) and Ang II had no additional effect, whereas it increased QOโ in wild-type. Addition of HโOโ reduced transport-dependent QOโ in wild-types, but not in p22(phox). Transport-independent QOโ was unaffected by HโOโ. The similar effects of Ang II and HโOโ to reduce transport-dependent QOโ suggest a direct regulatory role of oxidative stress. In accordance, the transport-dependent QOโ was reduced in p22(phox) already during baseline. The effects of Ang II on transport-independent QOโ was not replicated by HโOโ, indicating direct regulation via Ang II-receptors independently of oxidative stress. However, the Ang II effect was absent in p22(phox), suggesting that oxidative stress also modulates normal Ang II signaling. In conclusion, Ang II affects both transport-dependent and transport-independent QOโ in proximal tubular cells and may be an important pathway modulating renal QOโ.
โข O2k-Network Lab: US CO Denver Van Hove J, SE Uppsala Liss P
Labels: MiParea: Respiration, Genetic knockout;overexpression
Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Kidney, Other cell lines
HRR: Oxygraph-2k
noPDF