Evidence map›Paper›PMID 33494617›Full record

ArticleConnective tissue research2022

Regulation of chondrocyte biosynthetic activity by dynamic hydrostatic pressure: the role of TRP channels.

Alireza Savadipour, Robert J Nims, Dakota B Katz, Farshid Guilak

Open access · bronzeAbstract read
In one paragraph

Article in Connective tissue research, 2022. 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
3.4field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  6. NaNature · 2024
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  8. [Research progress of chondrocyte mechanotransduction mediated by TRPV4 and PIEZOs].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023
    Review
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  12. Mimicking Loading-Induced Cartilage Self-HeatingACS biomaterials science & engineering · 2023
    Article
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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 1 institution in 1 country.

Alireza SavadipourDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.ORCID 0000-0002-6395-6558
Robert J NimsDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.ORCID 0000-0002-0856-3188
Dakota B KatzDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.ORCID 0000-0001-8400-0582
Farshid GuilakDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.ORCID 0000-0001-7380-0330
Washington University in St. Louis · US

Funding

VISCOELASTIC PROPERTIES OF NORMAL AND OA CHONDRONSR01AG015768 · NIA · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 1998 to 2022
$7.7M
Washington University Rheumatic DiseasesResearch Resource-based CenterP30AR073752 · NIAMS · WASHINGTON UNIVERSITY · PI Megan Anne Cooper · 2018 to 2026
$7.6M
Resource Based Center for Musculoskeletal Biology and Medicine (Overall Application)P30AR074992 · NIAMS · WASHINGTON UNIVERSITY · PI MATTHEW J SILVA · 2019 to 2026
$6.8M
OBESITY, BIOMECHANICS, AND INFLAMMATION IN OSTEOARTHRITISR01AG046927 · NIA · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 2013 to 2023
$3.2M
Deconstructing Cartilage Mechanotransduction by Piezo ChannelsR01AR072999 · NIAMS · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 2020 to 2024
$2.9M
Mechanogenetic regulation of engineered tissuesR21AR076665 · NIAMS · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID · 2020 to 2021
$376k
Piezo channel activation and mechanotransduction in chondrocytes during traumatic injuryF32AR074240 · NIAMS · WASHINGTON UNIVERSITY · PI NIMS, ROBERT JOHN · 2018 to 2020
$196k
NIAMS NIH HHS F32 AR074240NIAMS NIH HHS P30 AR073752NIAMS NIH HHS P30 AR074992NIAMS NIH HHS R01 AR072999NIAMS NIH HHS R21 AR076665NIA NIH HHS R01 AG015768NIA NIH HHS R01 AG046927
6 · The paper itself

Abstract

introductionChondrocytes perceive and respond to mechanical loading as signals that regulate their metabolism. Joint loading exposes chondrocytes to multiple modes of mechanical stress, including hydrostatic pressure; however, the mechanisms by which chondrocytes sense physiologically relevant levels of hydrostatic pressure are not well understood. We hypothesized that hydrostatic pressure is transduced to an intracellular signal through mechanosensitive membrane ion channels of chondrocytes. The goals of this study were to examine the effect of hydrostatic loading on the development of engineered cartilage tissue and the contribution of mechanosensitive ion channels on these hydrostatic loading effects.

methodsUsing a 3D model of porcine chondrocytes in agarose, we applied specific chemical inhibitors to determine the role of transient receptor potential (TRP) ion channels TRPV1, TRPV4, TRPC3, and TRPC1 in transducing hydrostatic pressure.

resultsHydrostatic loading caused a frequency and magnitude-dependent decrease in sulfated glycosaminoglycans (S-GAG), without changes in DNA content. Inhibiting TRPC3 and TRPV4 decreased S-GAG content; however, only the inhibition of TRPV1 partially attenuated the hydrostatic loading-induced reduction in S-GAG content.

conclusionsOur findings indicate that TRPV1 may serve as a transducer of hydrostatic pressure in chondrocytes, and provide further support for the role of TRPV4 in regulating chondrocyte anabolism, as well as initial evidence implicating TRPC3 in chondrogenesis. These findings add to our further understanding of the chondrocyte "channelome" and suggest that a range of ion channels mediate the transduction of different biophysical stimuli such as hydrostatic pressure, membrane stretch, or osmotic stress.

Indexed as

Cartilage, ArticularTransient Receptor Potential ChannelsAnimalsCells, CulturedChondrocytesChondrogenesisGlycosaminoglycansHydrostatic PressureSwineTRPV Cation ChannelsGlycosaminoglycansTransient Receptor Potential ChannelsTRPV Cation ChannelscapsaicinMechanobiologyosteoarthritistissue engineering

Identifiers

PMID33494617
PMCPMC10061443
OpenAlexW3124057368

What OpenQuestion holds

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Read underepoch 390

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.