Evidence map›Paper›PMID 25796381›Full record

ArticleJournal of molecular neuroscience : MN2015

Estradiol Regulates Dorsal Vagal Complex Signal Transduction Pathway Transcriptional Reactivity to the AMPK Activator 5-Aminoimidazole-4-Carboxamide-Riboside (AICAR).

Fahaad S H Alenazi, Baher A Ibrahim, Karen P Briski

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

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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.

Fahaad S H AlenaziDepartment of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, 356 Bienville Building, 1800 Bienville Drive, Monroe, LA, 71201, USA.
Baher A IbrahimDepartment of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, 356 Bienville Building, 1800 Bienville Drive, Monroe, LA, 71201, USA.
Karen P BriskiDepartment of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, 356 Bienville Building, 1800 Bienville Drive, Monroe, LA, 71201, USA. briski@ulm.edu.
University of Louisiana at Monroe · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ovarian hormone estradiol (E) regulates effects of hindbrain adenosine 5'-monophosphate-activated protein kinase (AMPK) on caudal dorsal vagal complex (cDVC) neuron genomic activation and systemic glucostasis. The present study examined the hypothesis that cDVC signal transduction pathways exhibit distinctive E-dependent reactivity to activation of this sensor. RT-PCR microarray analysis was performed on RNA extracted from the cDVC of E- or oil (O)-implanted ovariectomized (OVX) adult female rats injected into the caudal fourth ventricle with the AMP mimetic 5-aminoimidazole-4-carboxamide-riboside (AICAR) (A) or saline (S). Microarray results show that the majority of marker genes differentially expressed in the E/S versus O/S cDVC were upregulated, as only myc (TGFβ; WNT pathways), bcl2 (Hedgehog pathway), and serpine (hypoxia pathway) mRNA profiles were downregulated by E. Several JAK/STAT and NFκB signaling pathway marker gene profiles were upregulated in O/A but unchanged in E/A; additional NFκB genes were inhibited by A in E but not O. Hypoxia and p53 pathways contain genes that were inhibited or stimulated in O/A, but unaltered in E/A. Conversely, TGFβ, p53, and NOTCH pathways each contained marker genes that were correspondingly modified or maintained in E/A versus O/A. Moreover, several oxidative stress pathway genes were suppressed in O/A while elevated or unchanged in E/A. Hedgehog, PPAR, and WNT signaling pathways were characterized by numerous examples of A-induced reversal of E augmentation of marker gene expression coinciding with opposite or no drug effects in O. Data presented here demonstrate that E exerts distinctive effects on cDVC signal transduction pathway marker gene reactivity to activated AMPK. Further research is needed to determine if observed changes in signal pathway marker gene transcription correlate with adjustments in gene product protein expression, and to characterize the role of aforementioned signaling pathways in E-sensitive cellular and systemic responses to hindbrain AMPK activation.

Indexed as

Second Messenger SystemsAminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsBrain StemEstradiolFemaleJanus KinasesNeuronsNF-kappa BProto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleyReceptors, NotchRibonucleotidesSerpinsAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesEstradiolJanus KinasesNF-kappa BProto-Oncogene Proteins c-bcl-2Receptors, NotchRibonucleotidesSerpinsSTAT Transcription FactorsTransforming Growth Factor betaTumor Suppressor Protein p53Wnt Proteins

Identifiers

PMID25796381
OpenAlexW2064325391

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.