Source:http://linkedlifedata.com/resource/pubmed/id/21511694
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2011-7-7
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| pubmed:abstractText |
The effects of TNF gene deletion on renal Na(+)-K(+)-2Cl(-) cotransporter (NKCC2) expression and activity were determined. Outer medulla from TNF(-/-) mice exhibited a twofold increase in total NKCC2 protein expression compared with wild-type (WT) mice. This increase was not observed in TNF(-/-) mice treated with recombinant human TNF (hTNF) for 7 days. Administration of hTNF had no effect on total NKCC2 expression in WT mice. A fourfold increase in NKCC2A mRNA accumulation was observed in outer medulla from TNF(-/-) compared with WT mice; NKCC2F and NKCC2B mRNA accumulation was similar between genotypes. The increase in NKCC2A mRNA accumulation was attenuated when TNF(-/-) mice were treated with hTNF. Bumetanide-sensitive O(2) consumption, an in vitro correlate of NKCC2 activity, was 2.8 ± 0.2 nmol·min(-1)·mg(-1) in medullary thick ascending limb tubules from WT, representing ?40% of total O(2) consumption, whereas, in medullary thick ascending limb tubules from TNF(-/-) mice, it was 5.6 ± 0.3 nmol·min(-1)·mg(-1), representing ?60% of total O(2) consumption. Administration of hTNF to TNF(-/-) mice restored the bumetanide-sensitive component to ?30% of total O(2) consumption. Ambient urine osmolality was higher in TNF(-/-) compared with WT mice (2,072 ± 104 vs. 1,696 ± 153 mosmol/kgH(2)O, P < 0.05). The diluting ability of the kidney, assessed by measuring urine osmolality before and after 1 h of water loading also was greater in TNF(-/-) compared with WT mice (174 ± 38 and 465 ± 81 mosmol/kgH(2)O, respectively, P < 0.01). Collectively, these findings suggest that TNF plays a role as an endogenous inhibitor of NKCC2 expression and function.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chlorides,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/Indicators and Reagents,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Chloride Symporters,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/sodium-potassium chloride...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
1522-1466
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
301
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
F94-100
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| pubmed:meshHeading |
pubmed-meshheading:21511694-Animals,
pubmed-meshheading:21511694-Blotting, Western,
pubmed-meshheading:21511694-Chlorides,
pubmed-meshheading:21511694-DNA, Complementary,
pubmed-meshheading:21511694-DNA Fragmentation,
pubmed-meshheading:21511694-Indicators and Reagents,
pubmed-meshheading:21511694-Isomerism,
pubmed-meshheading:21511694-Kidney Concentrating Ability,
pubmed-meshheading:21511694-Kidney Function Tests,
pubmed-meshheading:21511694-Kidney Medulla,
pubmed-meshheading:21511694-Male,
pubmed-meshheading:21511694-Mice,
pubmed-meshheading:21511694-Mice, Inbred C57BL,
pubmed-meshheading:21511694-Mice, Knockout,
pubmed-meshheading:21511694-Osmolar Concentration,
pubmed-meshheading:21511694-Oxygen Consumption,
pubmed-meshheading:21511694-RNA, Messenger,
pubmed-meshheading:21511694-Sodium-Potassium-Chloride Symporters,
pubmed-meshheading:21511694-Tumor Necrosis Factor-alpha
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| pubmed:year |
2011
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| pubmed:articleTitle |
Tumor necrosis factor-alpha is an endogenous inhibitor of Na+-K+-2Cl- cotransporter (NKCC2) isoform A in the thick ascending limb.
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| pubmed:affiliation |
Dept. of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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