Evidence map›Paper›PMID 29403560›Full record

ArticleOncology letters2018

Thrombopoietin protects H9C2 cells from excessive autophagy and apoptosis in doxorubicin-induced cardiotoxicity.

Han Wang, Hua Wang, En-Yu Liang, Li-Xia Zhou, Zhan-Ling Dong, Ping Liang, Qi-Fang Weng, Mo Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2018. 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
1.0field-weighted citation impact, top 22% 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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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 3 institutions in 1 country.

Han WangDepartment of Pediatrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Hua WangDepartment of Pediatrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
En-Yu LiangDepartment of Pediatrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Li-Xia ZhouDepartment of Pediatrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Zhan-Ling DongDepartment of Physiology, Hainan Medical College, Haikou, Hainan 571199, P.R. China.
Ping LiangDepartment of Physiology, Hainan Medical College, Haikou, Hainan 571199, P.R. China.
Qi-Fang WengDepartment of Physiology, Hainan Medical College, Haikou, Hainan 571199, P.R. China.
Mo YangDepartment of Pediatrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Southern Medical University · CNHainan Medical College Hospital · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac toxicity has been the major concern when using doxorubicin (DOX) in cancer therapy. Thrombopoietin (TPO) protects cardiac cells from DOX-induced cell damage; however, its molecular mechanism remains exclusive. The anti-autophagic and anti-apoptotic effects of TPO upon DOX treatment were studied in the cardiac H9C2 cell line, with bafilomycin A1 treatment as a positive control for autophagy inhibition. Cell viability was measured by Cell Counting Kit-8 assay in different treatment groups. The mRNA and/or protein levels of apoptotic markers and autophagy-associated factors were detected. The mean number of microtubule-associated protein 1A/1B-light chain 3 (LC3) puncta per cell was quantified to indicate autophagosomes and autolysosomes, of which the ones co-stained with lysosomal-associated membrane protein 1 were considered as autolysosomes. DOX treatment (5 µg/ml, 24 h) significantly impaired H9C2 cell viability compared with the control, while TPO pretreatment (10 ng/ml, 36 h) improved cell viability upon DOX treatment. DOX exposure markedly increased LC3 puncta in H9C2 cells, and TPO pretreatment reduced the number of autophagosomes, but showed no significant inhibitory effect on autolysosome formation. The autophagy inhibition by TPO upon DOX treatment was confirmed according to protein quantification of LC3-II and nucleoporin 62. TPO also suppressed autophagy-promoting protein Beclin-1, and elevated the anti-autophagic factors GATA-binding protein-4 and B cell lymphoma-2. Furthermore, TPO reduced DOX-induced apoptosis in H9C2 cells, as reflected by the amount changes of caspase-3. Taken together, these results revealed that TPO has a protective role in H9C2 cells from DOX-induced autophagy as well as apoptosis, and indicated that TPO may act as a cardioprotective drug in DOX-treated patients.

Indexed as

apoptosisautophagycardiotoxicitydoxorubicinthrombopoietin

Identifiers

PMID29403560
PMCPMC5780751
OpenAlexW2769951855

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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.