Evidence map›Paper›PMID 33431782›Full record

ArticleThe Kobe journal of medical sciences2020

Involvement of Receptor-Mediated S1P Signaling in EGF-Induced Macropinocytosis in COS7 Cells.

Shubi Ambwene Matovelo, Lifang Zhang, Nesma Nabil Ibrahim Mohamed, Taketoshi Kajimoto, Takeshi Ijuin, Taro Okada, Shun-Ichi Nakamura

Open access · greenAbstract read
In one paragraph

Article in The Kobe journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 3 countries.

Shubi Ambwene MatoveloDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Lifang ZhangDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Nesma Nabil Ibrahim MohamedDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Taketoshi KajimotoDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Takeshi IjuinDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Taro OkadaDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Shun-Ichi NakamuraDivision of Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Kobe University · JPAffiliated Hospital of Southwest Medical University · CNAin Shams University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macropinocytosis is a highly conserved cellular process of endocytosis by which extracellular fluid and nutrients are taken up into cells through large, heterogeneous vesicles known as macropinosomes. Growth factors such as epidermal growth factor (EGF) can induce macropinocytosis in many types of cells, although precise mechanism underlying EGF-induced macropinocytosis remains unclear. In the present studies we have shown the involvement of S1P signaling in EGF-induced macropinocytosis in COS7 cells. First, EGF-induced macropinocytosis was strongly impaired in sphingosine kinase isozymes, SphK1 or SphK2-depleted cells, which was completely rescued by the expression of the corresponding wild-type isozyme but not the catalytically inactive one, suggesting the involvement of sphingosine 1-phosphate (S1P) in this phenomenon. Next, we observed that EGF-induced macropinocytosis was strongly inhibited in S1P type 1 receptor (S1P1R)-knockdown cells, implying involvement of S1P1R in this event. Furthermore, we could successfully demonstrate EGF-induced trans-activation of S1P1R using one-molecular fluorescence resonance energy transfer (FRET) technique. Moreover, for EGF-induced Rac1 activation, a step essential to F-actin formation and subsequent macropinocytosis, S1P signaling is required for its full activation, as judged by FRET analysis. These findings indicate that growth factors such as EGF utilize receptor-mediated S1P signaling for the regulation of macropinocytosis to fulfil vital cell activity.

Indexed as

AnimalsChlorocebus aethiopsCOS CellsEpidermal Growth FactorFluorescence Resonance Energy TransferLysophospholipidsPinocytosisReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSignal TransductionSphingosineSphingosine-1-Phosphate ReceptorsEpidermal Growth FactorLysophospholipidsSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate ReceptorsEGFmacropinocytosisS1P receptorSphingosine 1-phosphatesphingosine kinase

Identifiers

PMID33431782
PMCPMC7837661
OpenAlexW3118250967

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.