Evidence map›Paper›PMID 21372146›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Gonadotropin-releasing hormone induces miR-132 and miR-212 to regulate cellular morphology and migration in immortalized LbetaT2 pituitary gonadotrope cells.

Joseph Godoy, Marin Nishimura, Nicholas J G Webster

Open access · greenAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Post-Transcriptional Regulation ofInternational journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. GnRH-A Key Regulator of FSH.Endocrinology · 2019
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. MicroRNA in teleost fish.Genome biology and evolution · 2014
    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 2 institutions in 1 country.

Joseph GodoyDepartment of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0673, USA.
Marin Nishimura
Nicholas J G Webster
University of California, San Diego · USVA San Diego Healthcare System · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
The Interaction of Neuroendocrine Repro. Function and Metabolic SignalingU54HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 1999 to 2013
$18.0M
The Role of FSH in Female InfertilityP50HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1985 to 2020
$7.5M
GnRH signaling in LbetaT2 gonadotrope cellsR01HD047400 · NICHD · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI WEBSTER, NICHOLAS J · 2005 to 2009
$1.3M
Alternative Splicing of the Insulin Receptor GeneI01BX000130 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI WEBSTER, NICHOLAS J · 2011 to 2013
–
BLRD VA I01 BX000130NCI NIH HHS P30 CA023100NICHD NIH HHS HD047400NICHD NIH HHS P50 HD012303NICHD NIH HHS R01 HD047400NICHD NIH HHS U54 HD012303NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

GnRH is central to the regulation of reproductive function. It acts on pituitary gonadotropes to stimulate LH and FSH synthesis and secretion. We had previously presented evidence for translational control of LHβ synthesis; therefore we investigated whether micro-RNAs might play a role in GnRH regulation in LβT2 cells. We show here that GnRH strongly induces the AK006051 gene transcript that encodes two micro-RNAs, miR-132 and miR-212, within the first intron. We show furthermore that the AK006051 promoter region is highly GnRH responsive. We verify that the p250Rho GTPase activating protein (GAP) is a target of miR-132/212 and show that GnRH treatment leads to a decrease in mRNA and protein expression. This reduction is blocked by an anti-miR to miR-132/212 and mimicked by a pre-miR-132. GnRH inhibits p250RhoGAP expression through a miR-132/212 response element within the 3'-untranslated region. The loss of p250RhoGAP expression leads to activation of Rac and marked increases in both the number and length of neurite-like processes extending from the cell. Knockdown of p250RhoGAP by small interfering RNA induces the same morphological changes observed with GnRH treatment. In addition, loss of p250RhoGAP causes an increase in cellular motility. Our findings suggest a novel pathway regulating long-term changes in cellular motility and process formation via the GnRH induction of miR-132/212 with the subsequent down-regulation of p250RhoGAP.

Indexed as

AnimalsBase SequenceCell Line, TransformedCell MovementCell ShapeExpressed Sequence TagsGene Expression ProfilingGonadotropin-Releasing HormoneGTPase-Activating ProteinsMiceMicroRNAsNeuritesOligonucleotide Array Sequence AnalysisPituitary GlandRNA InterferenceSequence AlignmentGonadotropin-Releasing HormoneGTPase-Activating ProteinsMicroRNAsMIRN132 microRNA, mouseMIRN212 microRNA, mouserho GTPase-activating protein

Identifiers

PMID21372146
PMCPMC3082323
OpenAlexW2077895664

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.