Evidence map›Paper›PMID 35770892›Full record

ArticleTissue engineering. Part A2022

Transcriptomic Regulation of Macrophages by Matrix-Bound Nanovesicle-Associated Interleukin-33.

Madeline Cramer, Catalina Pineda Molina, George Hussey, Heth R Turnquist, Stephen F Badylak

Open access · greenAbstract read
In one paragraph

Article in Tissue engineering. Part A, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 11 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

5 authors at 1 institution in 1 country.

Madeline CramerDepartment of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-8829-1468
Catalina Pineda MolinaMcGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0001-7710-6119
George HusseyMcGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Heth R TurnquistMcGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Stephen F BadylakDepartment of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
University of Pittsburgh · US

Funding

Immunoregulatory Mechanisms of IL-33 in Heart TransplantationR01HL122489 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Heth R Turnquist · 2015 to 2026
$4.9M
Mechanisms of functional skeletal muscle repair: critical role of matrix associated IL-33R01AR073527 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BADYLAK, STEPHEN F., TURNQUIST, HETH R · 2018 to 2022
$2.6M
Role of ECM-associated IL-33 in Functional Remodeling After Myocardial InfarctionF31HL151083 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CRAMER, MADELINE · 2020 to 2021
$72k
NHLBI NIH HHS F31 HL151083NHLBI NIH HHS R01 HL122489NIAMS NIH HHS R01 AR073527
6 · The paper itself

Abstract

The innate immune response, particularly the phenotype of responding macrophages, has significant clinical implications in the remodeling outcome following implantation of biomaterials and engineered tissues. In general, facilitation of an anti-inflammatory (M2-like) phenotype is associated with tissue repair and favorable outcomes, whereas pro-inflammatory (M1-like) activation can contribute to chronic inflammation and a classic foreign body response. Biologic scaffolds composed of extracellular matrix (ECM) and, more recently, matrix-bound nanovesicles (MBV) embedded within the ECM are known to direct macrophages toward an anti-inflammatory phenotype and stimulate a constructive remodeling outcome. The mechanisms of MBV-mediated macrophage activation are not fully understood, but interleukin-33 (IL-33) within the MBV appears critical for M2-like activation. Previous work has shown that IL-33 is encapsulated within the lumen of MBV and stimulates phenotypical changes in macrophages independent of its canonical surface receptor stimulation-2 (ST2). In the present study, we used next-generation RNA sequencing to determine the gene signature of macrophages following exposure to MBV with and without intraluminal IL-33. MBV-associated IL-33 instructed an anti-inflammatory phenotype in both wild-type and

Indexed as

Biological ProductsInterleukin-33Anti-Inflammatory AgentsBiocompatible MaterialsInterleukin-1 Receptor-Like 1 ProteinMacrophagesPhenotypeTranscriptomeAnti-Inflammatory AgentsBiocompatible MaterialsBiological ProductsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33extracellular matrixinterleukin-33macrophage phenotypematrix-bound nanovesicles

Identifiers

PMID35770892
PMCPMC9634988
OpenAlexW4283715169

What Socratic 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 Socratic graph.