Evidence map›Paper›PMID 22262018›Full record

ArticleJournal of cellular physiology2012

Bone marrow stromal cells stimulate an angiogenic program that requires endothelial MT1-MMP.

Suraj Kachgal, Bita Carrion, Isaac A Janson, Andrew J Putnam

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. The polymorphism MMP1 -1607 (1G>2G) is associated with a significantly increased risk of cancers from a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Pooled it
  2. Article
  3. Fibrin-based Bioinks: New Tricks from an Old Dog.International journal of bioprinting · 2020
    Review
  4. Article
  5. Review
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  7. Effects of CoClExperimental and therapeutic medicine · 2018
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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 2 institutions in 1 country.

Suraj KachgalDepartment of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA.
Bita Carrion
Isaac A Janson
Andrew J Putnam
University of California, Irvine · USUniversity of Michigan–Ann Arbor · US

Funding

Regulation and Enhancement of Angiogenesis in Dense Fibrin MatricesR01HL085339 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTNAM, ANDREW J · 2007 to 2024
$5.4M
NHLBI NIH HHS R01 HL085339
6 · The paper itself

Abstract

Bone marrow-derived stromal/stem cells (BMSCs) have recently been characterized as mediators of tissue regeneration after injury. In addition to preventing fibrosis at the wound site, BMSCs elicit an angiogenic response within the fibrin matrix. The mechanistic interactions between BMSCs and invading endothelial cells (ECs) during this process are not fully understood. Using a three-dimensional, fibrin-based angiogenesis model, we sought to investigate the proteolytic mechanisms by which BMSCs promote vessel morphogenesis. We find that BMSC-mediated vessel formation depends on the proteolytic ability of membrane type 1-matrix metalloproteinase (MT1-MMP). Knockdown of the protease results in a small network of vessels with enlarged lumens. Contrastingly, vessel morphogenesis is unaffected by the knockdown of MMP-2 and MMP-9. Furthermore, we find that BMSC-mediated vessel morphogenesis in vivo follows mechanisms similar to what we observe in vitro. Subcutaneous, cellular fibrin implants in C.B-17/SCID mice form aberrant vasculature when MMPs are inhibited with a broad-spectrum chemical inhibitor, and a very minimal amount of vessels when MT1-MMP proteolytic activity is interrupted in ECs. Other studies have debated the necessity of MT1-MMP in the context of vessel invasion in fibrin, but this study clearly demonstrates its requirement in BMSC-mediated angiogenesis.

Indexed as

Mesenchymal Stem CellsNeovascularization, PhysiologicAnimalsBone Marrow CellsCell CommunicationEndothelial CellsEnzyme InhibitorsFibrinGene Expression RegulationGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsMatrix Metalloproteinase 14Matrix Metalloproteinase 2Matrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsEnzyme InhibitorsFibrinMatrix Metalloproteinase 14Matrix Metalloproteinase 2Matrix Metalloproteinase 9Matrix Metalloproteinase Inhibitors

Identifiers

PMID22262018
PMCPMC3338896
OpenAlexW2127387931

What OpenQuestion holds

Textmetadata
LicenceTDM
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.