Evidence map›Paper›PMID 29934772›Full record

ArticleJournal of endocrinological investigation2019

Thyroid hormones act as mitogenic and pro survival factors in rat ovarian follicles.

R Canipari, C Mangialardo, V Di Paolo, F Alfei, S Ucci, V Russi, M G Santaguida, C Virili, M Segni, S Misiti and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Role of TInternational journal of molecular sciences · 2025
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  12. Impact of Thyroid Autoimmunity onFrontiers in endocrinology · 2021
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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

12 authors at 3 institutions in 1 country.

R CanipariDAHFMO, Unit of Histology and Medical Embryology, Sapienza, University of Rome, Rome, Italy.
C MangialardoDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy.
V Di PaoloDAHFMO, Unit of Histology and Medical Embryology, Sapienza, University of Rome, Rome, Italy.
F AlfeiDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy.
S UcciPasteur Institute of Rome, Rome, Italy.
V RussiPasteur Institute of Rome, Rome, Italy.
M G SantaguidaDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy.
C ViriliDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy.
M SegniDepartment of Pediatrics and Pediatric Neuropsychiatry, Sapienza, University of Rome, Rome, Italy.
S MisitiDepartment of Experimental Medicine, Sapienza, University of Rome, Rome, Italy.
M CentanniDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy.
C Verga FalzacappaDepartment of Medical-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Rome, Italy. cecilia.vergafalzacappa@uniroma1.it.
Sapienza University of Rome · ITIstituto Pasteur · ITBambino Gesù Children's Hospital · IT

Funding

Sapienza Università di Roma Ateneo Federato 2014-2015
6 · The paper itself

Abstract

purposeThyroid disorders are clinically associated with impaired fertility in women, and these abnormalities can be improved by restoring the euthyroid state. The exact mechanisms of thyroid effect on female fertility are not well known; however, it is conceivable that thyroid hormones (THs) might act on ovarian physiology via receptors in granulosa cells. This work is aimed at evaluating the effects of THs on non-tumoral granulosa cells and follicles.

methodsFreshly isolated rat ovarian follicles and granulosa cells were exposed to T3 or T4 (THs). Cell growth and viability were evaluated by cell counting and the MTT assay, respectively, follicle growth was evaluated by volume measurements. Apoptosis was evaluated by the TUNEL assay and active Caspase 3 staining. rGROV cells were exposed to T3, and apoptosis was induced by serum deprivation. Bcl2, Bcl-2-associated X protein (BAX), Akt and pAkt expression were evaluated by western blot.

resultsT3 induced a 40% increase in follicle volume (after 7 days). This increase was presumably due to the observed decrease (33%) in the apoptotic rate of the granulosa cell population. Both T3 and T4 caused a dose-dependent increase in rat granulosa cell number and viability. In addition, THs decreased the cell apoptotic rate in a dose-dependent manner. In both conditions, T3 appeared to be more efficient. In rGROV cells, 100 nM T3 induced cell growth and, in the absence of growth factors, reduced cell apoptosis by 40%, downregulating Caspase 3 and BAX. This effect was associated with an increase in pAkt levels. The involvement of the PI3 K pathway was confirmed by the ability of the PI3 K specific inhibitor (LY-294,002) to abolish T3 pro-survival action.

conclusionsTHs influence cell survival of ovarian granulosa cells. This effect likely contributes to the TH-induced follicle volume increase.

Indexed as

AnimalsApoptosisCell ProliferationCells, CulturedFemaleGranulosa CellsMitogensOvarian FollicleRatsRats, WistarThyroxineTriiodothyronineMitogensThyroxineTriiodothyronineApoptosisFolliclesGranulosa cellsOvaryThyroid hormones

Identifiers

PMID29934772
OpenAlexW2809075250

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.