Evidence map›Paper›PMID 21104120›Full record

ArticleAngiogenesis2011

Mesenchymal stem cells from adipose and bone marrow promote angiogenesis via distinct cytokine and protease expression mechanisms.

Suraj Kachgal, Andrew J Putnam

Abstract read
In one paragraph

Article in Angiogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 173 citations in OpenAlex.

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  15. State of the field: cellular and exosomal therapeutic approaches in vascular regeneration.American journal of physiology. Heart and circulatory physiology · 2022
    Review
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24 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Suraj KachgalDepartment of Biomedical Engineering, University of California, Irvine, CA 92697, USA. skachgal@umich.edu
Andrew J Putnam
University of California, Irvine · USUniversity of California System · 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

Using a fibrin-based angiogenesis model, we have established that there is no canonical mechanism used by endothelial cells (ECs) to degrade the surrounding extracellular matrix (ECM), but rather the set of proteases used is dependent on the mural cells providing the angiogenic cues. Mesenchymal stem cells (MSCs) originating from different tissues, which are thought to be phenotypically similar, promote angiogenesis through distinct mechanisms. Specifically, adipose-derived stem cells (ASCs) promote utilization of the plasminogen activator-plasmin axis by ECs as the primary means of vessel invasion and elongation in fibrin. Matrix metalloproteinases (MMPs) serve a purpose in regulating capillary diameter and possibly in stabilizing the nascent vessels. These proteolytic mechanisms are more akin to those involved in fibroblast-mediated angiogenesis than to those in bone marrow-derived stem cell (BMSC)-mediated angiogenesis. In addition, expression patterns of angiogenic factors such as urokinase plasminogen activator (uPA), hepatocyte growth factor (HGF), and tumor necrosis factor alpha (TNFα) were similar for ASC and fibroblast-mediated angiogenesis, and in direct contrast to BMSC-mediated angiogenesis. The present study illustrates that the nature of the heterotypic interactions between mural cells and endothelial cells depend on the identity of the mural cell used. Even MSCs which are shown to behave phenotypically similar do not stimulate angiogenesis via the same mechanisms.

Indexed as

Neovascularization, PhysiologicAdipose TissueBlood VesselsBone Marrow CellsCell DifferentiationCells, CulturedCoculture TechniquesCytokinesDipeptidesExtracellular MatrixFibrinolysinFibroblastsGene Expression ProfilingGene Expression RegulationHumansMatrix Metalloproteinase InhibitorsCytokinesDipeptidesFibrinolysinMatrix Metalloproteinase InhibitorsMatrix MetalloproteinasesN-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide

Identifiers

PMID21104120
PMCPMC3369878
OpenAlexW2016305198

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.