Evidence map›Paper›PMID 22539681›Full record

ArticleBiology of reproduction2012

Developmental programming: impact of prenatal testosterone excess on ovarian cell proliferation and apoptotic factors in sheep.

Natalia R Salvetti, Hugo H Ortega, Almudena Veiga-Lopez, Vasantha Padmanabhan

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Prenatal Androgen Excess Induces Multigenerational Effects on Female and Male Descendants.Clinical medicine insights. Endocrinology and diabetes · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Patients with polycystic ovary syndrome have successful embryo arrest.International journal of clinical and experimental medicine · 2015
    Article
  17. Early dexamethasone treatment induces placental apoptosis in sheep.Reproductive sciences (Thousand Oaks, Calif.) · 2015
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Natalia R SalvettiDepartment of Morphological Sciences, Faculty of Veterinary Sciences, National University of Litoral, Esperanza, Argentina.
Hugo H Ortega
Almudena Veiga-Lopez
Vasantha Padmanabhan
National University of the Littoral · ARUniversity of Michigan–Ann Arbor · US

Funding

STEROIDAL AND METABOLIC MEDIATION OF NEUROENDOCRINE CIRCUITRYP01HD044232 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PADMANABHAN, VASANTHA · 2004 to 2015
$12.9M
NICHD NIH HHS P01 HD044232NICHD NIH HHS P01-HD-44232
6 · The paper itself

Abstract

Prenatal testosterone (T) excess leads to reproductive dysfunctions in sheep, which include increased ovarian follicular recruitment and persistence. To test the hypothesis that follicular disruptions in T sheep stem from changes in the developmental ontogeny of ovarian proliferation and apoptotic factors, pregnant Suffolk sheep were injected twice weekly with T propionate or dihydrotestosterone propionate (DHT; a nonaromatizable androgen) from Days 30 to 90 of gestation. Changes in developmental expression of proliferating cell nuclear antigen (PCNA), BCL2, BAX, activated CASP3, and FAS/FASLG were determined at Fetal Days 90 and 140, 22 wk, 10 mo, and 21 mo of age by immunocytochemisty. Prenatal T treatment induced changes in expression of proliferative and apoptotic markers in a follicle-, age-, and steroid-specific manner. Changes in BAX were evident only during fetal life and PCNA, BCL2, and CASP3 only postnatally. Prenatal T and not DHT increased PCNA and decreased BCL2 in granulosa/theca cells of antral follicles at 10 and 21 mo but decreased CASP3 in granulosa/theca cells of antral follicles at 22 wk (prepubertal) and 10 and 21 mo. Both treatments decreased BAX immunostaining in granulosa cells of Fetal Day 90 primordial/primary follicles. Neither treatment affected FAS expression at any developmental time point in any follicular compartment. Effects on BAX appear to be programmed by androgenic actions and PCNA, BCL2, and CASP3 by estrogenic actions of T. Overall, the findings demonstrate that fetal exposure to excess T disrupts the ovarian proliferation/apoptosis balance, thus providing a basis for the follicular disruptions evidenced in these females.

Indexed as

AnimalsApoptosisCaspase 3Cell ProliferationDihydrotestosteroneFas Ligand Proteinfas ReceptorFemaleHumansOvaryPregnancyPrenatal Exposure Delayed EffectsProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2SheepTestosterone PropionateCaspase 3Dihydrotestosteronedihydrotestosterone propionateFas Ligand Proteinfas ReceptorProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2Testosterone Propionate

Identifiers

PMID22539681
PMCPMC3406557
OpenAlexW2163131117

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.