Evidence map›Paper›PMID 23340251›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

IGF-I signaling is essential for FSH stimulation of AKT and steroidogenic genes in granulosa cells.

Ping Zhou, Sarah C Baumgarten, Yanguang Wu, Jill Bennett, Nicola Winston, Jennifer Hirshfeld-Cytron, Carlos Stocco

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

  1. Growth hormone for in vitro fertilisation (IVF).The Cochrane database of systematic reviews · 2021
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Impact of Nutrition on Embryo Production in Cattle: Mechanistic Insights.Animals : an open access journal from MDPI · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

26 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Ping ZhouDepartments of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Sarah C Baumgarten
Yanguang Wu
Jill Bennett
Nicola Winston
Jennifer Hirshfeld-Cytron
Carlos Stocco
University of Illinois Chicago · US

Funding

TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
Molecular Pathways Controlling Ovarian Gene ExpressionR01HD057110 · NICHD · YALE UNIVERSITY · PI STOCCO, CARLOS OSCAR · 2009 to 2013
$1.5M
Regulation of Aromatase Expression in the Corpus LuteumR21HD066233 · NICHD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI STOCCO, CARLOS OSCAR · 2011 to 2012
$393k
NHLBI NIH HHS T32 HL007692NICHD NIH HHS R01 HD057110NICHD NIH HHS R01HD057110NICHD NIH HHS R21 HD066233NICHD NIH HHS R21HD066233
6 · The paper itself

Abstract

FSH and IGF-I synergistically stimulate gonadal steroid production; conversely, silencing the FSH or the IGF-I genes leads to infertility and hypogonadism. To determine the molecular link between these hormones, we examined the signaling cross talk downstream of their receptors. In human and rodent granulosa cells (GCs), IGF-I potentiated the stimulatory effects of FSH and cAMP on the expression of steroidogenic genes. In contrast, inhibition of IGF-I receptor (IGF-IR) activity or expression using pharmacological, genetic, or biochemical approaches prevented the FSH- and cAMP-induced expression of steroidogenic genes and estradiol production. In vivo experiments demonstrated that IGF-IR inactivation reduces the stimulation of steroidogenic genes and follicle growth by gonadotropins. FSH or IGF-I alone stimulated protein kinase B (PKB), which is also known as AKT and in combination synergistically increased AKT phosphorylation. Remarkably, blocking IGF-IR expression or activity decreased AKT basal activity and abolished AKT activation by FSH. In GCs lacking IGF-IR activity, FSH stimulation of Cyp19 expression was rescued by overexpression of constitutively active AKT. Our findings demonstrate, for the first time, that in human, mouse, and rat GCs, the well-known stimulatory effect of FSH on Cyp19 and AKT depends on IGF-I and on the expression and activation of the IGF-IR.

Indexed as

Signal TransductionAnimalsCell DifferentiationCyclic AMP Response Element-Binding ProteinEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleFollicle Stimulating HormoneGene Expression RegulationGranulosa CellsHEK293 CellsHumansInsulin-Like Growth Factor IMicePhosphorylationProto-Oncogene Proteins c-aktCyclic AMP Response Element-Binding ProteinExtracellular Signal-Regulated MAP KinasesFollicle Stimulating HormoneInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptors, FSHSteroids

Identifiers

PMID23340251
PMCPMC3589673
OpenAlexW2083574570

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.