Evidence map›Paper›PMID 29765419›Full record

ArticleStem cells international2018

Low Magnitude of Compression Enhances Biosynthesis of Mesenchymal Stem Cells towards Nucleus Pulposus Cells via the TRPV4-Dependent Pathway.

Yibo Gan, Bing Tu, Pei Li, Jixing Ye, Chen Zhao, Lei Luo, Chengmin Zhang, Zetong Zhang, Linyong Zhu, Qiang Zhou

Abstract read
In one paragraph

Article in Stem cells international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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  15. [Differential expression of transient receptor potential vanilloid receptor 4 protein in osteoarthritis and normal cartilages].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020
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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

10 authors.

Yibo GanNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.ORCID 0000-0002-6258-9100
Bing TuNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.
Pei LiDepartment of Orthopedic Surgery, No.89 Hospital of PLA, Weifang, 261026 Shandong, China.ORCID 0000-0001-9596-3122
Jixing YeNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.
Chen ZhaoNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.ORCID 0000-0003-4669-1874
Lei LuoNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.ORCID 0000-0001-7844-5921
Chengmin ZhangNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.ORCID 0000-0002-9913-111X
Zetong ZhangNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.
Linyong ZhuKey Laboratory for Advanced Materials, Institute of Fine Chemicals, East China University of Science and Technology, 130 Meilong Road, Shanghai 200237, China.
Qiang ZhouNational & Regional United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gao Tan Yan Street, Shapingba District, Chongqing 400038, China.ORCID 0000-0001-6253-329X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cell- (MSC-) based therapy is regarded as a promising tissue engineering strategy to achieve nucleus pulposus (NP) regeneration for the treatment of intervertebral disc degeneration (IDD). However, it is still a challenge to promote the biosynthesis of MSC to meet the requirement of NP regeneration. The purpose of this study was to optimize the compressive magnitude to enhance the extracellular matrix (ECM) deposition towards discogenesis of MSCs. Thus, we constructed a 3D culture model for MSCs to bear different magnitudes of compression for 7 days (5%, 10%, and 20% at the frequency of 1.0 Hz for 8 hours/day) using an intelligent and mechanically active bioreactor. Then, the underlying mechanotransduction mechanism of transient receptor potential vanilloid 4 (TRPV4) was further explored. The MSC-encapsulated hybrids were evaluated by Live/Dead staining, biochemical content assay, real-time PCR, Western blot, histological, and immunohistochemical analysis. The results showed that low-magnitude compression promoted anabolic response where high-magnitude compression induced the catabolic response for the 3D-cultured MSCs. The anabolic effect of low-magnitude compression could be inhibited by inhibiting TRPV4. Meanwhile, the activation of TRPV4 enhanced the biosynthesis analogous to low-magnitude compression. These findings demonstrate that low-magnitude compression promoted the anabolic response of ECM deposition towards discogenesis for the 3D-cultured MSCs and the TRPV4 channel plays a key role on mechanical signal transduction for low-magnitude compressive loading. Further understanding of this mechanism may provide insights into the development of new therapies for MSC-based NP regeneration.

Identifiers

PMID29765419
PMCPMC5932483

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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.