Evidence map›Paper›PMID 22128761›Full record

ArticleJournal of cellular and molecular medicine2012

Functional consequences of prolactin signalling in endothelial cells: a potential link with angiogenesis in pathophysiology?

Anne Q Reuwer, Patrycja Nowak-Sliwinska, Laurie A Mans, Chris M van der Loos, Jan H von der Thüsen, Marcel Th B Twickler, C Arnold Spek, Vincent Goffin, Arjan W Griffioen, Keren S Borensztajn

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

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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

10 authors at 5 institutions in 3 countries.

Anne Q ReuwerDepartment of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. a.q.reuwer@amc.uva.nl
Patrycja Nowak-Sliwinska
Laurie A Mans
Chris M van der Loos
Jan H von der Thüsen
Marcel Th B Twickler
C Arnold Spek
Vincent Goffin
Arjan W Griffioen
Keren S Borensztajn
Academic Medical Center · NLAmsterdam UMC Location VUmc · NLMedisch Centrum Haaglanden · NLUniversité Paris Cité · FRWaterlandziekenhuis · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolactin is best known as the polypeptide anterior pituitary hormone, which regulates the development of the mammary gland. However, it became clear over the last decade that prolactin contributes to a broad range of pathologies, including breast cancer. Prolactin is also involved in angiogenesis via the release of pro-angiogenic factors by leukocytes and epithelial cells. However, whether prolactin also influences endothelial cells, and whether there are functional consequences of prolactin-induced signalling in the perspective of angiogenesis, remains so far elusive. In the present study, we show that prolactin induces phosphorylation of ERK1/2 and STAT5 and induces tube formation of endothelial cells on Matrigel. These effects are blocked by a specific prolactin receptor antagonist, del1-9-G129R-hPRL. Moreover, in an in vivo model of the chorioallantoic membrane of the chicken embryo, prolactin enhances vessel density and the tortuosity of the vasculature and pillar formation, which are hallmarks of intussusceptive angiogenesis. Interestingly, while prolactin has only little effect on endothelial cell proliferation, it markedly stimulates endothelial cell migration. Again, migration was reverted by del1-9-G129R-hPRL, indicating a direct effect of prolactin on its receptor. Immunohistochemistry and spectral imaging revealed that the prolactin receptor is present in the microvasculature of human breast carcinoma tissue. Altogether, these results suggest that prolactin may directly stimulate angiogenesis, which could be one of the mechanisms by which prolactin contributes to breast cancer progression, thereby providing a potential tool for intervention.

Indexed as

Angiogenesis Inducing AgentsAnimalsBreast NeoplasmsCell LineChick EmbryoCollagenDrug CombinationsEndothelial CellsFemaleImmunohistochemistryLamininMAP Kinase Signaling SystemMiceNeovascularization, PathologicPhosphorylationProlactinAngiogenesis Inducing AgentsCollagenDrug CombinationsLamininmatrigelProlactinprolactin, Arg(129)-ProteoglycansReceptors, ProlactinSTAT5 Transcription Factor

Identifiers

PMID22128761
PMCPMC3822974
OpenAlexW2055352148

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.