Evidence map›Paper›PMID 24244341›Full record

ArticlePloS one2013

NF-κB and CREB are required for angiotensin II type 1 receptor upregulation in neurons.

Karla K V Haack, Amit K Mitra, Irving H Zucker

Expression of concernOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Mitochondrial CaJACC. Basic to translational science · 2024
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  12. Mechanisms Involved in Superiority of Angiotensin Receptor Blockade over ACE Inhibition in Attenuating Neuropathic Pain Induced in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. How Is the Brain Renin-Angiotensin System Regulated?Hypertension (Dallas, Tex. : 1979) · 2017
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Karla K V HaackDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Amit K Mitra
Irving H Zucker
University of Nebraska Medical Center · US

Funding

The Role of Excitatory Input into the PVN on Increased Sympathetic Drive in HeartP01HL062222 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SCHULTZ, HAROLD D · 1999 to 2019
$32.2M
NHLBI NIH HHS P01 HL062222PHS HHS P0-1 62222
6 · The paper itself

Abstract

Nuclear factor kappa B (NF-κB) and the Ets like gene-1 (Elk-1) are two transcription factors that have been previously established to contribute to the Angiotensin II mediated upregulation of Angiotensin II type 1 receptor (AT1R) in neurons. The cAMP response element binding protein (CREB) is another transcription factor that has also been implicated in AT1R gene transcription. The goal of the current study was to determine if NF-κB and CREB association was required for AT1R upregulation. We hypothesized that the transcription of the AT1R gene occurs via an orchestration of transcription factor interactions including NF-κB, CREB, and Elk-1. The synergistic role of CREB and NFκB in promoting AT1R gene expression was determined using siRNA-mediated silencing of CREB. Electrophorectic Mobility Shift Assay studies employing CREB and NF-κB demonstrated increased protein - DNA binding as a result of Ang II stimulation which was blunted by siRNA silencing of CREB. Upstream inhibition of p38 mitogen activated protein kinase (p38 MAPK) with SB203580 or inhibition of the calmodulin kinase (CAMK) pathway using KN-62 blunted changes in CREB and NF-κB expression. These findings suggest that Ang II may activate multiple signaling pathways involving p38 MAPK leading to the activation of NF-κB and CREB, which feed back to upregulate the AT1R gene. This study provides insight into the molecular mechanisms involving multiple transcription factor activation in a coordinated fashion which may be partially responsible for sympathoexcitation in clinical conditions associated with increased activation of the renin angiotensin system.

Indexed as

Angiotensin IIAnti-Inflammatory Agents, Non-SteroidalCell LineCyclic AMP Response Element-Binding Proteinets-Domain Protein Elk-1HumansImidazolesNF-kappa Bp38 Mitogen-Activated Protein KinasesPyridinesReceptor, Angiotensin, Type 1Up-RegulationVasoconstrictor AgentsAngiotensin IIAnti-Inflammatory Agents, Non-SteroidalCREB1 protein, humanCyclic AMP Response Element-Binding ProteinELK1 protein, humanets-Domain Protein Elk-1ImidazolesNF-kappa Bp38 Mitogen-Activated Protein KinasesPyridinesReceptor, Angiotensin, Type 1SB 203580Vasoconstrictor Agents

Identifiers

PMID24244341
PMCPMC3823855
OpenAlexW2021321063

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.