Linked Life Data

15454393

Source:http://linkedlifedata.com/resource/pubmed/id/15454393

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-7
pubmed:abstractText
X-linked hypophosphatemia is the most common inherited form of rickets. It is characterized by renal phosphate wasting, leading to hypophosphatemia and an inappropriately normal or low serum level of 1,25(OH)2 vitamin D. Previous studies have pointed to a circulating factor or phosphatonin-inhibiting phosphate transport by decreasing mRNA of the proximal tubule NaP(i) cotransporter NaPi-2A. The present study examined the hypothesis that there was also posttranscriptional regulation of the NaPi-2A cotransporter in Hyp mice proximal tubules and whether the phosphate transport defect in Hyp mice persisted when they were studied in vitro. We found that the rate of phosphate transport in Hyp mice was <50% that in C57/B6 control mice. While phosphate transport remained stable during incubation with time in C57/B6 mice proximal tubules, it increased from 0.46 +/- 0.47 to 1.83 +/- 0.40 pmol x mm(-1) x min(-1) in Hyp proximal tubules (P < 0.01) consistent with phosphatonin washout in Hyp proximal tubules perfused in vitro. This time-dependent increase in phosphate transport was still observed in the presence of cycloheximide. There was also a reduction of proximal tubule apical NaPi-2A expression from Hyp mice compared with C57/B6 mice using single-tubule immunohistochemistry. Using immunohistochemistry, we demonstrate an increase in apical expression of the NaPi-2A transporter in proximal tubules perfused in vitro in Hyp mice even in the presence of bath cycloheximide. The increase in apical expression of the NaPi-2A transporter in proximal tubules perfused in vitro in Hyp mice was blocked by colchicine. These data are consistent with a rapidly reversible posttranscriptional defect in Hyp mice causing a reduction in phosphate transport.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F363-70
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:15454393-Adsorption, pubmed-meshheading:15454393-Animals, pubmed-meshheading:15454393-Disease Models, Animal, pubmed-meshheading:15454393-Gene Expression Regulation, pubmed-meshheading:15454393-Humans, pubmed-meshheading:15454393-Hypophosphatemia, Familial, pubmed-meshheading:15454393-Immunohistochemistry, pubmed-meshheading:15454393-Kidney Tubules, Proximal, pubmed-meshheading:15454393-Male, pubmed-meshheading:15454393-Mice, pubmed-meshheading:15454393-Phosphate Transport Proteins, pubmed-meshheading:15454393-Phosphates, pubmed-meshheading:15454393-Protein Processing, Post-Translational, pubmed-meshheading:15454393-Sodium-Phosphate Cotransporter Proteins, pubmed-meshheading:15454393-Sodium-Phosphate Cotransporter Proteins, Type IIa, pubmed-meshheading:15454393-Symporters
pubmed:year
2005
pubmed:articleTitle
Phosphatonin washout in Hyp mice proximal tubules: evidence for posttranscriptional regulation.
pubmed:affiliation
Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75235-9063, USA. Michel.Baum@UTSouthwestern.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.