Evidence map›Paper›PMID 36692671›Full record

ArticleHuman cell2023

Regulatory role of apelin receptor signaling in migration and differentiation of mouse embryonic stem cell-derived mesoderm cells and mesenchymal stem/stromal cells.

Hatice Burcu Şişli, Selinay Şenkal, Taha Bartu Hayal, Ezgi Bulut, Ayşegül Doğan

Abstract read
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In one paragraph

Article in Human cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-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

6 citing papers in PubMed, 9 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

5 authors at 1 institution in 1 country.

Hatice Burcu ŞişliFaculty of Engineering, Genetics and Bioengineering Department, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-6528-8365
Selinay ŞenkalFaculty of Engineering, Genetics and Bioengineering Department, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-6897-7307
Taha Bartu HayalFaculty of Engineering, Genetics and Bioengineering Department, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-1369-2715
Ezgi BulutFaculty of Engineering, Genetics and Bioengineering Department, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-5842-6088
Ayşegül DoğanFaculty of Engineering, Genetics and Bioengineering Department, Yeditepe University, Istanbul, Turkey. aysegul.dogan@yeditepe.edu.tr.ORCID http://orcid.org/0000-0003-4160-2270
Yeditepe University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesoderm-derived cells, including bone, muscle, and mesenchymal stem/stromal cells (MSCs), constitute various parts of vertebrate body. Cell therapy with mesoderm specification in vitro may be a promising treatment for diseases affecting organs of mesodermal origin. Repair and regeneration of damaged organs with in vitro generation of mesoderm-derived tissues and MSCs hold a great potential for regenerative therapy. Therefore, understanding the signaling pathways involving mesoderm and mesoderm-derived cellular differentiation is important. Previous findings indicated the importance of Apelin receptor (Aplnr) signaling, during embryonic development, in gastrulation, cell migration, and differentiation. Nevertheless, regulatory role of Aplnr pathway in differentiation of mesoderm and mesoderm-derived MSCs remains unclear. In the current study, we tried to elucidate the role of Aplnr signaling during mesoderm cell migration and differentiation from mouse embryonic stem cells (mESCs). By activating and suppressing Aplnr signaling pathway via peptide, small molecule, and genetic modifications including siRNA- and shRNA-mediated knockdown and CRISPR-Cas9-mediated knockout (KO), we revealed that Aplnr signaling not only induces migration of cells during germ layer formation but also enhances mesoderm differentiation through FGF/MAPK pathway. Antibody array and LC/MS protein profiling data demonstrated that Apelin-13 treatment enhanced cell cycle, EGFR, FGF, Wnt, and Integrin signaling pathway proteins. Furthermore, Aplelin-13 treatment improved MSC characteristics, with mesenchymal phenotype and high expression of MSC markers, and silencing Aplnr signaling components resulted in significantly reduced expression of MSC markers. Also, Aplnr signaling activity enhanced proliferation and survival of the cells during MSC derivation from mesoderm.

Indexed as

Mouse Embryonic Stem CellsSignal TransductionAnimalsApelin ReceptorsCell DifferentiationFemaleMesodermMicePregnancyStromal CellsApelin ReceptorsAplnr protein, mouseApelin-13Apelin receptorElabelaEmbryonic stem cellsMesenchymal stem/stromal cells

Identifiers

PMID36692671
OpenAlexW4317870160

What OpenQuestion holds

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Registered trials

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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.