Evidence map›Paper›PMID 30876926›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology2019

Thrombospondin-2 regulates extracellular matrix production, LOX levels, and cross-linking via downregulation of miR-29.

N E Calabro, A Barrett, A Chamorro-Jorganes, S Tam, N J Kristofik, Hao Xing, Ayomiposi M Loye, W C Sessa, K Hansen, T R Kyriakides

Open access · greenAbstract read
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The Role of Thrombospondin-2 in Myocardial Fibrosis.Drug design, development and therapy · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Targeting hypoxia and thrombospondin-2 in diabetic wound healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  12. Review
  13. Emerging therapeutic targets in systemic sclerosis.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Driving adult tissue repair via re-engagement of a pathway required for fetal healing.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  18. Article
  19. Article
  20. Article
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 at 2 institutions in 1 country.

N E CalabroInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT 06510, USA.
A BarrettDepartment of Biochemistry and Molecular Genetics, Biological Mass Spectrometry Facility, University of Colorado Denver, Aurora, CO 80045, USA.
A Chamorro-JorganesInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
S TamInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA.
N J KristofikInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Biomedical Engineering, School of Engineering and Applied Science, Yale University, New Haven, CT 06511, USA.
Hao XingInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Biomedical Engineering, School of Engineering and Applied Science, Yale University, New Haven, CT 06511, USA.
Ayomiposi M LoyeInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Biomedical Engineering, School of Engineering and Applied Science, Yale University, New Haven, CT 06511, USA.
W C SessaInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.
K HansenDepartment of Biochemistry and Molecular Genetics, Biological Mass Spectrometry Facility, University of Colorado Denver, Aurora, CO 80045, USA.
T R KyriakidesInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Biomedical Engineering, School of Engineering and Applied Science, Yale University, New Haven, CT 06511, USA. Electronic address: themis.kyriakides@yale.edu.
Yale University · USUniversity of Colorado Denver · US

Funding

Surgery / Physiology CoreP01HL107205 · NHLBI · YALE UNIVERSITY · PI SIMONS, MICHAEL · 2012 to 2022
$18.8M
MCP-1 and attenuation of the foreign body responseR01GM072194 · NIGMS · YALE UNIVERSITY · PI KYRIAKIDES, THEMIS R · 2005 to 2018
$4.7M
NHLBI NIH HHS P01 HL107205NIGMS NIH HHS R01 GM072194
6 · The paper itself

Abstract

Collagen fibrillogenesis and crosslinking have long been implicated in extracellular matrix (ECM)-dependent processes such as fibrosis and scarring. However, the extent to which matricellular proteins influence ECM protein production and fibrillar collagen crosslinking has yet to be determined. Here we show that thrombospondin 2 (TSP2), an anti-angiogenic matricellular protein, is an important modulator of ECM homeostasis. Specifically, through a fractionated quantitative proteomics approach, we show that loss of TSP2 leads to a unique ECM phenotype characterized by a significant decrease in fibrillar collagen, matricellular, and structural ECM protein production in the skin of TSP2 KO mice. Additionally, TSP2 KO skin displays decreased lysyl oxidase (LOX), which manifests as an increase in fibrillar collagen solubility and decreased levels of LOX-mediated fibrillar collagen crosslinking. We show that these changes are indirectly mediated by miR-29, a major regulator of ECM proteins and LOX, as miR-29 expression is increased in the TSP2 KO. Altogether, these findings indicate that TSP2 contributes to ECM production and assembly by regulating miR-29 and LOX.

Indexed as

AnimalsCollagenDown-RegulationExtracellular MatrixExtracellular Matrix ProteinsGene Knockout TechniquesMaleMiceMicroRNAsProtein-Lysine 6-OxidaseProteomicsThrombospondin 2ThrombospondinsCollagenExtracellular Matrix ProteinsLox protein, mouseMicroRNAsMIRN29 microRNA, mouseProtein-Lysine 6-OxidaseThrombospondin 2ThrombospondinsCollagenExtracellular matrixLysyl oxidasemiR-29ProteomicsThrombospondin 2

Identifiers

PMID30876926
PMCPMC6710120
OpenAlexW2922263673

What OpenQuestion holds

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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.