Evidence map›Paper›PMID 26378412›Full record

ArticleCell cycle (Georgetown, Tex.)2015

Binding of FGF2 to FGFR2 in an autocrine mode in trophectoderm cells is indispensable for mouse blastocyst formation through PKC-p38 pathway.

Jing Yang, Dan Zhang, Ying Yu, Run-Ju Zhang, Xiao-Ling Hu, He-Feng Huang, Yong-Chao Lu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  5. Expression Analysis ofBiology · 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

7 authors at 3 institutions in 1 country.

Jing Yanga Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
Dan Zhanga Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
Ying Yua Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
Run-Ju Zhanga Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
Xiao-Ling Hua Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
He-Feng Huangb The Key Laboratory of Reproductive Genetics, Ministry of Education, Zhejiang University ; Hangzhou, Zhejiang , China.
Yong-Chao Lua Department of Reproductive Endocrinology ; Women's Hospital, Zhejiang University School of Medicine ; Hangzhou, Zhejiang , China.
Women's Hospital, School of Medicine, Zhejiang University · CNZhejiang University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factors (FGF1, FGF2 and FGF4) and fibroblast growth factor receptors (FGFR1, FGFR2, FGFR3 and FGFR4) have been reported to be expressed in preimplantation embryos and be required for their development. However, the functions of these molecules in trophectoderm cells (TEs) that lead to the formation of the blastocyst as well as the underlying mechanism have not been elucidated. The present study has demonstrated for the first time that endogenous FGF2 secreted by TEs can regulate protein expression and distribution in TEs via the FGFR2-mediated activation of PKC and p38, which are important for the development of expanded blastocysts. This finding provides the first explanation for the long-observed phenomenon that only high concentrations of exogenous FGFs have effects on embryonic development, but in vivo the amount of endogenous FGFs are trace. Besides, the present results suggest that FGF2/FGFR2 may act in an autocrine fashion and activate the downstream PKC/p38 pathway in TEs during expanded blastocyst formation.

Indexed as

AnimalsAutocrine CommunicationBlastocystEctodermFemaleFibroblast Growth Factor 2HumansMAP Kinase Signaling SystemMiceMice, Inbred ICRPregnancyProtein BindingProtein Kinase CReceptor, Fibroblast Growth Factor, Type 2Fgfr2 protein, mouseFibroblast Growth Factor 2Protein Kinase CReceptor, Fibroblast Growth Factor, Type 2blastocyst formationfibroblast growth factor 2 (FGF2)fibroblast growth factor receptor 2 (FGFR2)p38 MAPKprotein kinase C (PKC)

Identifiers

PMID26378412
PMCPMC4825582
OpenAlexW2257709668

What Socratic 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 Socratic graph.