Evidence map›Paper›PMID 23293787›Full record

ArticleLife sciences2012

Extracellular signal-regulated kinases 1/2 signaling pathways are not involved in endothelin regulation of mouse inner medullary collecting duct nitric oxide production.

Kelly A Hyndman, Alexander H MacDonell, Jennifer S Pollock

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  2. High dietary sodium causes dyssynchrony of the renal molecular clock in rats.American journal of physiology. Renal physiology · 2018
    Article
  3. Article
  4. Article
  5. High salt induces autocrine actions of ET-1 on inner medullary collecting duct NO production via upregulated ETB receptor expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  6. Endothelin.Pharmacological reviews · 2016
    Review
  7. Dynamin-2 is a novel NOS1β interacting protein and negative regulator in the collecting duct.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  8. Article
  9. Review
  10. Article
  11. Nitric oxide and the A and B of endothelin of sodium homeostasis.Current opinion in nephrology and hypertension · 2013
    Review
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

3 authors at 1 institution in 1 country.

Kelly A HyndmanSection of Experimental Medicine, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA 30912, United States.
Alexander H MacDonell
Jennifer S Pollock
Augusta University · US

Funding

Renal endothelin receptor-specific function in angiotensin ll-dependent hypertensP01HL095499 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2010 to 2014
$11.1M
Nitric Oxide Synthase Isoforms in the KidneyR01HL060653 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI POLLOCK, JENNIFER S · 1999 to 2010
$2.5M
NHLBI NIH HHS HL60653NHLBI NIH HHS HL95499NHLBI NIH HHS P01 HL095499NHLBI NIH HHS R01 HL060653
6 · The paper itself

Abstract

aimsTo determine if endothelin-1 (ET-1) stimulates the phosphorylation of ERK1/2 in the mouse inner medullary collecting duct (IMCD), and if this in turn upregulates nitric oxide (NO) production. MAIN

methodsConfluent mouse IMCD segment-3 cells (mIMCD-3) were stimulated with 50 nM ET-1 for24 h with and without various doses of ET receptor antagonists, BQ123 (ETA antagonist,) or BQ788 (ETB antagonist) and phosphorylation of ERK1/2 determined by immunoblots. As well, NOS isoform expression and nitrite production were assessed. Finally, increasing doses of the MEK inhibitors, PD98,059 or U0126,were incubated with mIMCD-3 cells and the ET-1 dependent nitrite production determined. KEY

findingsET-1 via the ETB receptor significantly increased ERK1/2 phosphorylation, and was prevented by MEK inhibition. ET-1 also stimulates nitrite production by mIMCD-3 cells (basal: 54.5±26 pmol/mg pr/hvs ET-1: 221±28 pmol/mg pr/h; N=4) via the ETB receptor (BQ788+ET-1: 83.7±27 pmol/mg pr/h);however, ET-1 does not regulate NOS1 or NOS3 expression. MEK inhibition did not prevent the ET-1 stimulated nitrite production contrary to our initial hypothesis (vehicle+ET-1: 157±13 pmol/mg pr/hr vs PD98,059+ET-1: 305.7±24 pmol/mg pr/h, N=4, P>0.05). SIGNIFICANCE: Although the mouse IMCD-3 cells only express the NOS1β splice variant, ET-1 did regulate mouse IMCD nitrite production. ET-1 stimulates ERK1/2 phosphorylation in the mouse IMCD, but ERK1/2 signaling is not involved in the ET-1 dependent increase in NO production by IMCD cells. Thus, we propose that ET-1 regulates protein–protein interactions that are necessary for NO production, that are independent of MAPK signaling cascades.

Indexed as

AnimalsEndothelin-1ImmunoblottingKidney MedullaKidney Tubules, CollectingMAP Kinase Signaling SystemMiceNitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IIIPeptides, CyclicPhosphorylationSignal TransductionUp-Regulationcyclo(Trp-Asp-Pro-Val-Leu)Endothelin-1Nitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IIINos1 protein, mouseNos3 protein, mousePeptides, Cyclic

Identifiers

PMID23293787
PMCPMC3897254
OpenAlexW1981545914

What OpenQuestion holds

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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.