Evidence map›Paper›PMID 25808356›Full record

ArticleStem cells and development2015

A Paracrine Mechanism Accelerating Expansion of Human Induced Pluripotent Stem Cell-Derived Hepatic Progenitor-Like Cells.

Kota Tsuruya, Hiromi Chikada, Kinuyo Ida, Kazuya Anzai, Tatehiro Kagawa, Yutaka Inagaki, Tetsuya Mine, Akihide Kamiya

Abstract read
In one paragraph

Article in Stem cells and development, 2015. 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
0.9field-weighted citation impact, top 26% 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, 13 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

8 authors at 1 institution in 1 country.

Kota Tsuruya1 Laboratory of Stem Cell Therapy, Institute of Innovative Science and Technology, Tokai University , Isehara, Japan .
Hiromi Chikada1 Laboratory of Stem Cell Therapy, Institute of Innovative Science and Technology, Tokai University , Isehara, Japan .
Kinuyo Ida1 Laboratory of Stem Cell Therapy, Institute of Innovative Science and Technology, Tokai University , Isehara, Japan .
Kazuya Anzai1 Laboratory of Stem Cell Therapy, Institute of Innovative Science and Technology, Tokai University , Isehara, Japan .
Tatehiro Kagawa2 Division of Gastroenterology, Department of Internal Medicine, School of Medicine, Tokai University , Isehara, Japan .
Yutaka Inagaki3 Department of Regenerative Medicine, School of Medicine and Center for Matrix Biology and Medicine, Graduate School of Medicine, Tokai University , Isehara, Japan .
Tetsuya Mine2 Division of Gastroenterology, Department of Internal Medicine, School of Medicine, Tokai University , Isehara, Japan .
Akihide Kamiya1 Laboratory of Stem Cell Therapy, Institute of Innovative Science and Technology, Tokai University , Isehara, Japan .
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic stem/progenitor cells in liver development have a high proliferative potential and the ability to differentiate into both hepatocytes and cholangiocytes. In this study, we focused on the cell surface molecules of human induced pluripotent stem (iPS) cell-derived hepatic progenitor-like cells (HPCs) and analyzed how these molecules modulate expansion of these cells. Human iPS cells were differentiated into immature hepatic lineage cells by cytokines. In addition to hepatic progenitor markers (CD13 and CD133), the cells were coimmunostained for various cell surface markers (116 types). The cells were analyzed by flow cytometry and in vitro colony formation culture with feeder cells. Twenty types of cell surface molecules were highly expressed in CD13(+)CD133(+) cells derived from human iPS cells. Of these molecules, CD221 (insulin-like growth factor receptor), which was expressed in CD13(+)CD133(+) cells, was quickly downregulated after in vitro expansion. The proliferative ability was suppressed by a neutralizing antibody and specific inhibitor of CD221. Overexpression of CD221 increased colony-forming ability. We also found that inhibition of CD340 (erbB2) and CD266 (fibroblast growth factor-inducible 14) signals suppressed proliferation. In addition, both insulin-like growth factor (a ligand of CD221) and tumor necrosis factor-like weak inducer of apoptosis (a ligand of CD266) were provided by feeder cells in our culture system. This study revealed the expression profiles of cell surface molecules in human iPS cell-derived HPCs and that the paracrine interactions between HPCs and other cells through specific receptors are important for proliferation.

Indexed as

3T3 CellsAnimalsBile DuctsBiomarkersCell Culture TechniquesCell DifferentiationCell LineCell ProliferationCytokinesErb-b2 Receptor Tyrosine KinasesFeeder CellsFibroblast Growth FactorsFlow CytometryHepatocytesHumansInduced Pluripotent Stem CellsBiomarkersCytokinesErb-b2 Receptor Tyrosine Kinasesfibroblast growth factor 14Fibroblast Growth FactorsMembrane ProteinsReceptor, IGF Type 1Receptors, SomatomedinReceptors, Tumor Necrosis FactorSomatomedinsTNFRSF12A protein, humanTWEAK Receptor

Identifiers

PMID25808356
PMCPMC4499795
OpenAlexW2062628660

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.