Evidence map›Paper›PMID 32323761›Full record

ArticleMolecular medicine reports2020

The roles of mechanosensitive ion channels and associated downstream MAPK signaling pathways in PDLC mechanotransduction.

Yun Shen, Yongchu Pan, Shuyu Guo, Lian Sun, Chi Zhang, Lin Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 51 citations in OpenAlex.

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  19. Dentin Mechanobiology: Bridging the Gap between Architecture and Function.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

6 authors at 1 institution in 1 country.

Yun ShenInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yongchu PanInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Shuyu GuoInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Lian SunInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Chi ZhangInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Lin WangInstitute of Stomatology, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate whether the cytoskeleton, the Piezo1 ion channel and the transient receptor potential cation channel subfamily V member 4 (TRPV4) ion channel are equally functional in the mechanotransduction of periodontal ligament cells (PDLCs) and to reveal the interplay of these mechanically sensitive ion channels (MSCs). Human PDLCs (hPDLCs) were pretreated with cytochalasin D (the inhibitor of actin polymerization), GsMTx4 (the antagonist of Piezo1) and GSK205 (the antagonist of TRPV4), and then subjected to periodic mechanical loading. The expression levels of macrophage colony stimulating factor (M‑CSF), receptor activator of NF‑κB ligand (RANKL) and cyclooxygenase‑2 (COX2) in hPDLCs were detected via western blotting. Osteoblast mineralization induction capacity of the hPDLCs was also studied and the mitogen‑activated protein kinase (MAPK) expression profile was determined via protein microarray. The expression of Piezo1 and TRPV4 in the PDLCs was significantly increased at 8 h after loading. These differences in expression were accompanied by increased expression of M‑CSF, RANKL and COX2. Compared with the control group, key PDLC biomarkers were suppressed after mechanical loading following treatment with the inhibitors of Piezo1 (GsMTx4) and TRPV4 (GSK205). The phosphorylated‑MAPK protein array showed differential biomarker profiles among all groups. The present study suggested that both MSCs and the cytoskeleton participated as mechanical sensors, and did so independently in hPDLC mechanotransduction. Furthermore, the Piezo1 ion channel may transmit mechanical signals via the ERK signaling pathway; however, the TRPV4 channel may function via alternative signaling pathways.

Indexed as

AdolescentAnimalsCells, CulturedChildCyclooxygenase 2Cytochalasin DFemaleHumansIntercellular Signaling Peptides and ProteinsIon ChannelsMacrophage Colony-Stimulating FactorMAP Kinase Signaling SystemMechanotransduction, CellularMiceMice, Inbred BALB COsteoblastsCSF1 protein, humanCyclooxygenase 2Cytochalasin DIntercellular Signaling Peptides and ProteinsIon ChannelsMacrophage Colony-Stimulating FactorMTx4 protein, Grammostola spatulataPIEZO1 protein, humanRANK LigandSpider VenomsTNFSF11 protein, humanTRPV4 protein, humanTRPV Cation Channelsmechanotransductionmitogen-activated protein kinase pathwayperiodontal ligament cellsPiezo1transient receptor potential cation channel subfamily V member 4

Identifiers

PMID32323761
PMCPMC7115221
OpenAlexW3007617812

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.