Evidence map›Paper›PMID 19323981›Full record

ArticleMicrovascular research2009

Inhibition of angiogenesis in vitro: a central role for beta-actin dependent cytoskeletal remodeling.

Jennifer T Durham, Ira M Herman

Open access · greenAbstract read
In one paragraph

Article in Microvascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  16. Bioactive peptides derived from vascular endothelial cell extracellular matrices promote microvascular morphogenesis and wound healing in vitro.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    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

2 authors at 1 institution in 1 country.

Jennifer T DurhamDepartment of Physiology, Tufts University School of Medicine, Boston, MA 02111, USA.
Ira M Herman
Tufts University · US

Funding

PATHOBIOLOGY OF DIGESTIVE DISEASEST32DK007542 · NIDDK · TUFTS UNIVERSITY BOSTON · PI LISCUM, LAURA · 1986 to 2010
$3.5M
Regulating retinal microvascular morphogenesisR01EY015125 · NEI · TUFTS UNIVERSITY BOSTON · PI HERMAN, IRA M · 2004 to 2010
$1.7M
RETINAL MICROVASCULAR CELLS, MATRIX, &OCULAR DISORDERSR01EY009033 · NEI · TUFTS UNIVERSITY BOSTON · PI HERMAN, IRA M · 1993 to 2002
$817k
NEI NIH HHS EY 15125NEI NIH HHS R01 EY009033NEI NIH HHS R01 EY015125NIDDK NIH HHS T32 DK007542NIDDK NIH HHS T32 DK07542
6 · The paper itself

Abstract

Endothelial cell migration and proliferation, central steps in both physiologic and pathologic angiogenesis, require cytoskeletal-dependent remodeling, which is, in large part, achieved by the dynamic regulation of the beta-actin network. Specifically, the beta-actin network has previously been shown to be (i) enriched in regions of highly motile cytoplasm, and (ii) modulated by its isoactin-specific barbed-end capping protein, beta cap73. We hypothesize that regulated over-expression of beta cap73 could disrupt angiogenesis by capping beta-actin-filament assembly thus inhibiting the incipient cellular migration and microvascular morphogenesis that ensues. Indeed, upon infection of capillary endothelial cells (cEC) with an adenovirus encoding the full-length beta cap73 (Ad-beta cap73), there is a robust cellular rounding response that occurs concomitantly with cytoskeletal disruption, as visualized with immunofluorescence microscopy. Further, we demonstrate that over-expression of Ad-beta cap73 inhibits cEC migration in wound healing studies. Quantitative in vitro angiogenesis assays reveal that Ad-beta cap73 not only prevents endothelial cells from forming capillary-like networks, but also induces the collapse of preformed endothelial tubes. In testing whether Ad-beta cap73 impairs angiogenic events by inducing anoikis/apoptosis, we demonstrate that beta cap73 infection activates a caspase-3-mediated cell death response as observed by quantitative Western blotting and immunofluorescence analyses. Altogether, these findings suggest that endothelial-specific targeting and beta cap73 over-expression may represent an innovative therapeutic approach capable of abrogating pathologic angiogenesis.

Indexed as

Angiogenesis InhibitorsAnimalsAnoikisCapillariesCapZ Actin Capping ProteinCattleCell MovementCells, CulturedCytoskeletonEndothelium, VascularExtracellular MatrixNeovascularization, PathologicRNA, MessengerSignal TransductionWound HealingAngiogenesis InhibitorsCapZ Actin Capping ProteinRNA, Messenger

Identifiers

PMID19323981
PMCPMC2706787
OpenAlexW2011343445

What OpenQuestion holds

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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.