Evidence map›Paper›PMID 16099864›Full record

ArticleEndocrinology2005

Estrogens up-regulate the Fas/FasL apoptotic pathway in lactotropes.

G Jaita, M Candolfi, V Zaldivar, S Zárate, L Ferrari, D Pisera, M G Castro, A Seilicovich

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 43 citations in OpenAlex.

  1. Promoter polymorphism of FASL confers protection against female-specific cancers and those of FAS impact the cancers divergently.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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  8. Fas receptor is required for estrogen deficiency-induced bone loss in mice.Laboratory investigation; a journal of technical methods and pathology · 2010
    Article
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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

8 authors at 2 institutions in 2 countries.

G JaitaCentro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Piso 10, Buenos Aires (C1121ABG), Argentina.
M Candolfi
V Zaldivar
S Zárate
L Ferrari
D Pisera
M G Castro
A Seilicovich
University of Buenos Aires · ARCedars-Sinai Medical Center · US

Funding

Gene therapy for chronic neurodegenerative disordersR01NS044556 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2002 to 2006
$2.0M
APOPTOSIS OF ANTERIOR PITUITARY CELLSR03TW006273 · FIC · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2004 to 2006
$102k
FIC NIH HHS 1R03-TW006273-01A1FIC NIH HHS R03 TW006273NINDS NIH HHS 1R01-NS44556NINDS NIH HHS R01 NS044556
6 · The paper itself

Abstract

The Fas/FasL system provides the major apoptotic mechanism for many cell types, participating in cell turnover in hormone-dependent tissues. In the present study, we localized both Fas and FasL in anterior pituitary cells, mainly in lactotropes and somatotropes. The percentage of anterior pituitary cells showing immunoreactivity for Fas or FasL was higher in cells from rats killed in proestrus than in diestrus. Also, the proportion of pituitary cells from ovariectomized (OVX) rats expressing Fas or FasL increased in the presence of 17beta-estradiol (10(-9) M). This steroid increased the percentage of lactotropes with immunoreactivity for Fas or FasL and the percentage of somatotropes expressing Fas. Activation of Fas by an agonist anti-Fas antibody (Mab-Fas) decreased the vi-ability-3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT assay)-of anterior pituitary cells from OVX rats cultured in the presence of 17beta-estradiol. Also, membrane-bound FasL decreased cell viability-[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] assay (MTS assay)-only when anterior pituitary cells from OVX rats were incubated with 17beta-estradiol. Moreover, FasL increased the percentage of hypodiploid anterior pituitary cells (flow cytometry). Mab-Fas increased the percentage of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL)-positive pituitary cells and lactotropes from OVX rats only when cells were incubated in the presence of 17beta-estradiol. Also, Mab-Fas triggered apoptosis of anterior pituitary cells from rats killed at proestrus but not at diestrus. Our results show that 17beta-estradiol up-regulates the expression of the Fas/FasL system in anterior pituitary cells and increases Fas-induced apoptosis in lactotropes, suggesting that Fas-induced apoptosis could be involved in the pituitary cell renewal during the estrous cycle.

Indexed as

AnimalsApoptosisDiestrusEstradiolEstrogensFas Ligand Proteinfas ReceptorFemaleMembrane GlycoproteinsOvariectomyPituitary Gland, AnteriorProestrusProlactinRatsRats, WistarTumor Necrosis FactorsEstradiolEstrogensFaslg protein, ratFas Ligand Proteinfas ReceptorMembrane GlycoproteinsProlactinTumor Necrosis Factors

Identifiers

PMID16099864
PMCPMC1266288
OpenAlexW1976507766

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.