Evidence map›Paper›PMID 17015841›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaCl.

Morgan Gallazzini, Joan D Ferraris, Margarita Kunin, Ryan G Morris, Maurice B Burg

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 56 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Article
  2. Article
  3. International journal of molecular sciences · 2025
    Article
  4. Article
  5. Article
  6. Current Knowledge on Mammalian Phospholipase AMolecules (Basel, Switzerland) · 2022
    Review
  7. Updating Phospholipase ABiomolecules · 2020
    Review
  8. NFAT5, which protects against hypertonicity, is activated by that stress via structuring of its intrinsically disordered domain.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Phosphatidylcholine and the CDP-choline cycle.Biochimica et biophysica acta · 2013
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Morgan GallazziniLaboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Department of Health and Human Services, Bethesda, MD 20892-1603, USA. gallazzinim@nhlbi.nih.gov
Joan D Ferraris
Margarita Kunin
Ryan G Morris
Maurice B Burg
National Heart Lung and Blood Institute · US

Funding

ROLE OF ORGANIC OSMOLYTES IN RENAL CELLSZ01HL001283 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BURG, MAURICE BENJAM · 1988 to 2008
$3.8M
Response Of Renal Cells To Osmotic StressZIAHL001283 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BURG, MAURICE BENJAM · 2009 to 2010
$3.5M
6 · The paper itself

Abstract

Glycerophosphocholine (GPC) is an osmoprotective compatible and counteracting organic osmolyte that accumulates in renal inner medullary cells in response to high NaCl and urea. We previously found that high NaCl increases GPC in renal [Madin-Darby canine kidney (MDCK)] cells. The GPC is derived from phosphatidylcholine, catalyzed by a phospholipase that was not identified at that time. Neuropathy target esterase (NTE) was recently shown to be a phospholipase B that catalyzes production of GPC from phosphatidylcholine. The purpose of the present study was to test whether NTE contributes to the high NaCl-induced increase of GPC synthesis in renal cells. We find that in mouse inner medullary collecting duct cells, high NaCl increases NTE mRNA within 8 h and NTE protein within 16 h. Diisopropyl fluorophosphate, which inhibits NTE esterase activity, reduces GPC accumulation, as does an siRNA that specifically reduces NTE protein abundance. The 20-h half-life of NTE mRNA is unaffected by high NaCl. TonEBP/OREBP is a transcription factor that is activated by high NaCl. Knockdown of TonEBP/OREBP by a specific siRNA inhibits the high NaCl-induced increase of NTE mRNA. Further, the lower renal inner medullary interstitial NaCl concentration that occurs chronically in ClCK1-/- mice and acutely in normal mice given furosemide is associated with lower NTE mRNA and protein. We conclude that high NaCl increases transcription of NTE, likely mediated by TonEBP/OREBP, and that the resultant increase of NTE expression contributes to increased production and accumulation of GPC in mammalian renal cells in tissue culture and in vivo.

Indexed as

AnimalsCarboxylic Ester HydrolasesCell LineGlycerylphosphorylcholineKidneyMiceSodium ChlorideWater-Electrolyte BalanceCarboxylic Ester HydrolasesGlycerylphosphorylcholineneurotoxic esteraseSodium Chloride

Identifiers

PMID17015841
PMCPMC1622810
OpenAlexW2064293313

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.