Evidence map›Paper›PMID 35659731›Full record

ArticleStem cell research & therapy2022

Hyperthermia increases HSP production in human PDMCs by stimulating ROS formation, p38 MAPK and Akt signaling, and increasing HSF1 activity.

Ju-Fang Liu, Po-Chun Chen, Thai-Yen Ling, Chun-Han Hou

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  14. Heat shock proteins in hypothermia: a review.Frontiers in molecular biosciences · 2025
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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 4 institutions in 1 country.

Ju-Fang Liu *School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Po-Chun Chen *Department of Life Science, National Taiwan Normal University, Taipei, 116, Taiwan.
Thai-Yen LingGraduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, 106, Taiwan.
Chun-Han HouDepartment of Orthopedic Surgery, National Taiwan University Hospital, No. 1, Jen-Ai Road, Taipei, 100, Taiwan. chhou@ntu.edu.tw.ORCID 0000-0002-3850-0997
China Medical University · TWNational Taiwan Normal University · TWNational Taiwan University · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman placenta-derived multipotent cells (hPDMCs) are isolated from a source uncomplicated by ethical issues and are ideal for therapeutic applications because of their capacity for multilineage differentiation and proven immunosuppressive properties. It is known that heat shock preconditioning induces the upregulation of heat shock proteins (HSPs), which enhance survival and engraftment of embryonic stem cells (ESCs) during transplantation in live animal models, although whether heat shock preconditioning has the same effects in hPDMCs is unclear.

methodsThe hPDMCs were isolated from placenta of healthy donors. The cells were treated with heat shock (43 °C, 15 min), followed by evaluation of cell viability. Furthermore, the HSPs expression was assessed by Western blot, qPCR. The reactive oxygen species (ROS) production and signal pathway activation were determined by flow cytometry and Western blot, respectively. The regulatory pathways involved in HSPs expression were examined by pretreatment with chemical inhibitors, and siRNAs of MAPK, Akt, and heat shock factor 1 (HSF1), followed by determination of HSPs expression.

resultsThis study demonstrates that heat shock treatment induced ROS generation and HPSs expression in hPDMCs. Heat shock stimulation also increased p38 MAPK and Akt phosphorylation. These effects were reduced by inhibitors of ROS, p38 MAPK and Akt. Moreover, we found that heat shock treatment enhanced nuclear translocation of the HSF1 in hPDMCs, representing activation of HSF1. Pretreatment of hPDMCs with ROS scavengers, SB203580 and Akt inhibitors also reduced the translocation of HSF1 induced by heat shock.

conclusionsOur data indicate that heat shock acts via ROS to activate p38 MAPK and Akt signaling, which subsequently activates HSF1, leading to HSP activation and contributing to the protective role of hPDMCs.

Indexed as

Hyperthermia, Inducedp38 Mitogen-Activated Protein KinasesAnimalsDNA-Binding ProteinsHeat-Shock ProteinsHeat Shock Transcription FactorsHSP70 Heat-Shock ProteinsHumansProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionTranscription FactorsDNA-Binding ProteinsHeat-Shock ProteinsHeat Shock Transcription FactorsHSP70 Heat-Shock Proteinsp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTranscription FactorsHeat shockHeat shock proteins (HSPs)hPDMCs (hPDMCs)

Identifiers

PMID35659731
PMCPMC9166587
OpenAlexW4281719093

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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.