Evidence map›Paper›PMID 28638990›Full record

ArticleAngiogenesis2017

Pharmacological intervention of MKL/SRF signaling by CCG-1423 impedes endothelial cell migration and angiogenesis.

David Gau, William Veon, Teresa L Capasso, Ralph Bottcher, Sanjeev Shroff, Beth L Roman, Partha Roy

Open access · greenAbstract read
In one paragraph

Article in Angiogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  4. Rho/SRF Inhibitor Modulates Mitochondrial Functions.International journal of molecular sciences · 2022
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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

7 authors at 2 institutions in 2 countries.

David GauDepartment of Bioengineering, University of Pittsburgh, 306 CNBIO, 300 Technology Drive, Pittsburgh, PA, 15219, USA.
William VeonDepartment of Bioengineering, University of Pittsburgh, 306 CNBIO, 300 Technology Drive, Pittsburgh, PA, 15219, USA.
Teresa L CapassoDepartment of Human Genetics, University of Pittsburgh, Pittsburgh, PA, USA.
Ralph BottcherDepartment of Molecular Medicine, Max-Planck Institute of Biochemistry, Martinsried, Germany.
Sanjeev ShroffDepartment of Bioengineering, University of Pittsburgh, 306 CNBIO, 300 Technology Drive, Pittsburgh, PA, 15219, USA.
Beth L RomanDepartment of Human Genetics, University of Pittsburgh, Pittsburgh, PA, USA.
Partha RoyDepartment of Bioengineering, University of Pittsburgh, 306 CNBIO, 300 Technology Drive, Pittsburgh, PA, 15219, USA. Partha.Roy@pitt.edu.
University of Pittsburgh · USMax Planck Institute of Biochemistry · DE

Funding

Cardiovascular Bioengineering Training ProgramT32HL076124 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANJEEV G SHROFF · 2005 to 2026
$7.0M
Profilin as a target to suppress Invasive breast cancerR01CA108607 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROY, PARTHA · 2006 to 2017
$2.6M
NCI NIH HHS R01 CA108607NHLBI NIH HHS T32 HL076124
6 · The paper itself

Abstract

De novo synthesis of cytoskeleton-regulatory proteins triggered by the megakaryoblastic leukemia (MKL)/serum response factor (SRF) transcriptional system in response to pro-angiogenic growth factors lies at the heart of endothelial cell (EC) migration (a critical element of angiogenesis) and neovascularization. This study explores whether pharmacological intervention of MKL/SRF signaling axis by CCG-1423 is able to suppress angiogenesis. Our studies show that CCG-1423 inhibits migration and cord morphogenesis of EC in vitro and sprouting angiogenesis ex vivo and in vivo, suggesting CCG-1423 could be a novel anti-angiogenic agent. Kymography analyses of membrane dynamics of EC revealed that CCG-1423 treatment causes a major defect in membrane protrusion. CCG-1423 treatment led to attenuated expression of several actin-binding proteins that are important for driving membrane protrusion including ArpC2, VASP, and profilin1 (Pfn1) with the most drastic effect seen on the expression of Pfn1. Finally, depletion of Pfn1 alone is also sufficient for a dramatic decrease in sprouting angiogenesis of EC in vitro and ex vivo, further suggesting that Pfn1 depletion may be one of the mechanisms of the anti-angiogenic action of CCG-1423.

Indexed as

ActinsAngiogenesis InhibitorsAnilidesAnimalsBenzamidesCell LineCell MovementCell Surface ExtensionsEmbryo, NonmammalianEndothelial CellsHumansMice, KnockoutNeovascularization, PhysiologicProfilinsSerum Response FactorSignal TransductionActinsAngiogenesis InhibitorsAnilidesBenzamidesCCG 1423MRTFA protein, humanProfilinsSerum Response FactorTrans-ActivatorsAngiogenesisArpC2CCG-1423Cell migrationConditional knockoutEndothelial cellsProfilin-1VASP

Identifiers

PMID28638990
PMCPMC5985144
OpenAlexW2661568919

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.