Evidence map›Paper›PMID 31017799›Full record

ArticleAmerican journal of physiology. Cell physiology2019

Matrix stiffness regulates microvesicle-induced fibroblast activation.

Samantha C Schwager, Francois Bordeleau, Jian Zhang, Marc A Antonyak, Richard A Cerione, Cynthia A Reinhart-King

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 52 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

6 authors at 2 institutions in 1 country.

Samantha C SchwagerDepartment of Biomedical Engineering, Vanderbilt University , Nashville, Tennessee.
Francois BordeleauDepartment of Biomedical Engineering, Vanderbilt University , Nashville, Tennessee.
Jian ZhangDepartment of Biomedical Engineering, Vanderbilt University , Nashville, Tennessee.ORCID 0000-0003-2887-6082
Marc A AntonyakDepartment of Biomedical Science, Cornell University , Ithaca, New York.
Richard A CerioneDepartment of Biomedical Science, Cornell University , Ithaca, New York.
Cynthia A Reinhart-KingDepartment of Biomedical Engineering, Vanderbilt University , Nashville, Tennessee.
Vanderbilt University · USCornell University · US

Funding

The unique roles of the GTP-binding/protein crosslinking enzyme transglutaminase-2 and signaling partners in aggressive cancersR01CA201402 · NCI · CORNELL UNIVERSITY · PI CERIONE, RICHARD A. · 2016 to 2024
$4.3M
Alternative splicing regulation by extracellular matrix mechanics: a self-tuning tool to control cell microenvironmental adaptation and tumor progressionK99CA212270 · NCI · VANDERBILT UNIVERSITY · PI BORDELEAU, FRANCOIS · 2017 to 2018
$225k
NCI NIH HHS K99 CA212270NCI NIH HHS R01 CA201402
6 · The paper itself

Abstract

Extracellular vesicles released by cancer cells have recently been implicated in the differentiation of stromal cells to their activated, cancer-supporting states. Microvesicles, a subset of extracellular vesicles released from the plasma membrane of cancer cells, contain biologically active cargo, including DNA, mRNA, and miRNA, which are transferred to recipient cells and induce a phenotypic change in behavior. While it is known that microvesicles can alter recipient cell phenotype, little is known about how the physical properties of the tumor microenvironment affect fibroblast response to microvesicles. Here, we utilized cancer cell-derived microvesicles and synthetic substrates designed to mimic the stiffness of the tumor and tumor stroma to investigate the effects of microvesicles on fibroblast phenotype as a function of the mechanical properties of the microenvironment. We show that microvesicles released by highly malignant breast cancer cells cause an increase in fibroblast spreading, α-smooth muscle actin expression, proliferation, cell-generated traction force, and collagen gel compaction. Notably, our data indicate that these phenotypic changes occur only on stiff matrices mimicking the stiffness of the tumor periphery and are dependent on the cell type from which the microvesicles are shed. Overall, these results show that the effects of cancer cell-derived microvesicles on fibroblast activation are regulated by the physical properties of the microenvironment, and these data suggest that microvesicles may have a more robust effect on fibroblasts located at the tumor periphery to influence cancer progression.

Indexed as

Mechanotransduction, CellularParacrine CommunicationActinsAnimalsBreast NeoplasmsCancer-Associated FibroblastsCell-Derived MicroparticlesCell ProliferationElastic ModulusExtracellular MatrixFemaleHumansMCF-7 CellsMiceNIH 3T3 CellsPhenotypeActa2 protein, mouseActinscell contractilityextracellular matrixfibroblast activationmechanotransductiontraction force

Identifiers

PMID31017799
PMCPMC6689748
OpenAlexW2941141634

What OpenQuestion holds

Textmetadata
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.