Evidence map›Paper›PMID 33805444›Full record

ArticleInternational journal of molecular sciences2021

Withholding of M-CSF Supplement Reprograms Macrophages to M2-Like via Endogenous

Yu-Chih Chen, Yin-Siew Lai, Yan-Der Hsuuw, Ko-Tung Chang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  19. T Regulatory Cell Subsets Do Not Restore for One Year After Acute COVID-19.International journal of molecular sciences · 2024
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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

4 authors at 1 institution in 1 country.

Yu-Chih ChenGraduate Institute of Bioresources, National Pingtung University of Science and Technology, Pingtung 91201, Taiwan.
Yin-Siew LaiResearch Center for Animal Biologics, National Pingtung University of Science and Technology, Pingtung 91201, Taiwan.ORCID 0000-0003-2963-9038
Yan-Der HsuuwDepartment of Tropical Agriculture and International Cooperation, Pingtung 91201, Taiwan.
Ko-Tung ChangResearch Center for Animal Biologics, National Pingtung University of Science and Technology, Pingtung 91201, Taiwan.ORCID 0000-0001-9383-831X
National Pingtung University of Science and Technology · TW

Funding

Ministry of Science and Technology, Taiwan MOST 106-2314-B-020-001, MOST 107-2731-M-020-001, MOST 108-3017-F-020-001, MOST 108-2731-M-020 -001, MOST 108-2314-B-020-002, MOST 109-2634-F-020-001 and MOST 109-2314-B-020-002
6 · The paper itself

Abstract

Macrophage colony-stimulating factor (M-CSF or CSF-1) is known to have a broad range of actions on myeloid cells maturation, including the regulation of macrophage differentiation, proliferation and survival. Macrophages generated by M-CSF stimulus have been proposed to be alternatively activated or M2 phenotype. M-CSF is commonly overexpressed by tumors and is also known to enhance tumor growth and aggressiveness via stimulating pro-tumor activities of tumor-associated macrophages (TAMs). Currently, inhibition of CSF-1/CSF-1R interaction by therapeutic antibody to deplete TAMs and their pro-tumor functions is becoming a prevalent strategy in cancer therapy. However, its antitumor activity shows a limited single-agent effect. Therefore, macrophages in response to M-CSF interruption are pending for further investigation. To achieve this study, bone marrow derived macrophages were generated in vitro by M-CSF stimulation for 7 days and then continuously grown until day 21 in M-CSF absence. A selective pressure for cell survival was initiated after withdrawal of M-CSF. The surviving cells were more prone to M2-like phenotype, even after receiving interleukin-4 (IL-4) stimulation. The transcriptome analysis unveiled that endogenous

Indexed as

AnimalsCells, CulturedCell SurvivalCellular ReprogrammingFemaleGene Expression RegulationLectins, C-TypeMacrophage Colony-Stimulating FactorMacrophagesMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BLReceptors, Cell SurfaceReceptors, Granulocyte-Macrophage Colony-Stimulating FactorTumor-Associated MacrophagesCSF1 protein, mouseCsf1r protein, mouseLectins, C-TypeMacrophage Colony-Stimulating FactorMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceReceptors, Granulocyte-Macrophage Colony-Stimulating FactorM2-likemacrophageM-CSFtranscriptome

Identifiers

PMID33805444
PMCPMC8037162
OpenAlexW3148442542

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.