Evidence map›Paper›PMID 34226523›Full record

ArticleCell death discovery2021

Methyltransferase-like protein 7A (METTL7A) promotes cell survival and osteogenic differentiation under metabolic stress.

Eugene Lee, Ju-Young Kim, Tae-Kyung Kim, Seo-Young Park, Gun-Il Im

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Extended lifespan and improved genome stability in HepaRG-derived cell lines through reprogramming by high-density stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  14. A Novel Localization of METTL7A in Bergmann Glial Cells in Human Cerebellum.International journal of molecular sciences · 2023
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  17. METTLing in Stem Cell and Cancer Biology.Stem cell reviews and reports · 2023
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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.

Eugene LeeResearch Institute for Integrative Regenerative Biomedical Engineering, Dongguk University, Goyang, 10326, Republic of Korea.
Ju-Young KimResearch Institute for Integrative Regenerative Biomedical Engineering, Dongguk University, Goyang, 10326, Republic of Korea.
Tae-Kyung KimResearch Institute for Integrative Regenerative Biomedical Engineering, Dongguk University, Goyang, 10326, Republic of Korea.
Seo-Young ParkResearch Institute for Integrative Regenerative Biomedical Engineering, Dongguk University, Goyang, 10326, Republic of Korea.
Gun-Il ImResearch Institute for Integrative Regenerative Biomedical Engineering, Dongguk University, Goyang, 10326, Republic of Korea. imgunil@hanmail.net.ORCID http://orcid.org/0000-0002-6953-2326
Dongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While bone has an inherent capacity to heal itself, it is very difficult to reconstitute large bone defects. Regenerative medicine, including stem cell implantation, has been studied as a novel solution to treat these conditions. However, when the local vascularity is impaired, even the transplanted cells undergo rapid necrosis before differentiating into osteoblasts and regenerating bone. Thus, to increase the effectiveness of stem cell transplantation, it is quintessential to improve the viability of the implanted stem cells. In this study, given that the regulation of glucose may hold the key to stem cell survival and osteogenic differentiation, we investigated the molecules that can replace the effect of glucose under ischemic microenvironment of stem cell transplantation in large bone defects. By analyzing differentially expressed genes under glucose-supplemented and glucose-free conditions, we explored markers such as methyltransferase-like protein 7A (METTL7A) that are potentially related to cell survival and osteogenic differentiation. Overexpression of METTL7A gene enhanced the osteogenic differentiation and viability of human bone marrow stem cells (hBMSCs) in glucose-free conditions. When the in vivo effectiveness of METTL7A-transfected cells in bone regeneration was explored in a rat model of critical-size segmental long-bone defect, METTL7A-transfected hBMSCs showed significantly better regenerative potential than the control vector-transfected hBMSCs. DNA methylation profiles showed a large difference in methylation status of genes related to osteogenesis and cell survival between hBMSCs cultured in glucose-supplemented condition and those cultured in glucose-free condition. Interestingly, METTL7A overexpression altered the methylation status of related genes to favor osteogenic differentiation and cell survival. In conclusion, it is suggested that a novel factor METTL7A enhances osteogenic differentiation and viability of hBMSCs by regulating the methylation status of genes related to osteogenesis or survival.

Identifiers

PMID34226523
PMCPMC8257615
OpenAlexW3181927400

What OpenQuestion holds

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LicenceCC BY
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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.