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Mature and progenitor endothelial cells perform angiogenesis also under protease inhibition: the amoeboid angiogenesis

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, April 2018
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  • Above-average Attention Score compared to outputs of the same age (63rd percentile)
  • Above-average Attention Score compared to outputs of the same age and source (64th percentile)

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Title
Mature and progenitor endothelial cells perform angiogenesis also under protease inhibition: the amoeboid angiogenesis
Published in
Journal of Experimental & Clinical Cancer Research, April 2018
DOI 10.1186/s13046-018-0742-2
Pubmed ID
Authors

Anastasia Chillà, Francesca Margheri, Alessio Biagioni, Mario Del Rosso, Gabriella Fibbi, Anna Laurenzana

Abstract

Controlling vascular growth is a challenging aim for the inhibition of tumor growth and metastasis. The amoeboid and mesenchymal types of invasiveness are two modes of migration interchangeable in cancer cells: the Rac-dependent mesenchymal migration requires the activity of proteases; the Rho-ROCK-dependent amoeboid motility is protease-independent and has never been described in endothelial cells. A cocktail of physiologic inhibitors (Ph-C) of serine-proteases, metallo-proteases and cysteine-proteases, mimicking the physiological environment that cells encounter during their migration within the angiogenesis sites was used to induce amoeboid style migration of Endothelial colony forming cells (ECFCs) and mature endothelial cells (ECs). To evaluate the mesenchymal-ameboid transition RhoA and Rac1 activation assays were performed along with immunofluorescence analysis of proteins involved in cytoskeleton organization. Cell invasion was studied in Boyden chambers and Matrigel plug assay for the in vivo angiogenesis. In the present study we showed in both ECFCs and ECs, a decrease of activated Rac1 and an increase of activated RhoA upon shifting of cells to the amoeboid conditions. In presence of Ph-C inhibitors both cell lines acquired a round morphology and Matrigel invasion was greatly enhanced with respect to that observed in the absence of protease inhibition. We also observed that the urokinase-plasminogen-activator (uPAR) receptor silencing and uPAR-integrin uncoupling with the M25 peptide abolished both mesenchymal and amoeboid angiogenesis of ECFCs and ECs in vitro and in vivo, indicating a role of the uPAR-integrin-actin axis in the regulation of amoeboid angiogenesis. Furthermore, under amoeboid conditions endothelial cells seem to be indifferent to VEGF stimulation, which induces an amoeboid signaling pattern also in mesenchymal conditions. Here we first provide a data set disclosing that endothelial cells can move and differentiate into vascular structures in vitro and in vivo also in the absence of proteases activity, performing a new type of neovascularization: the "amoeboid angiogenesis". uPAR is indispensable for ECs and ECFCs to perform an efficient amoeboid angiogenesis. Therefore, uPAR silencing or the block of its integrin-interaction, together with standard treatment against VEGF, could be a possible solution for angiogenesis inhibition.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 22 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 18%
Student > Bachelor 3 14%
Other 2 9%
Lecturer 1 5%
Professor 1 5%
Other 3 14%
Unknown 8 36%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 32%
Medicine and Dentistry 4 18%
Nursing and Health Professions 1 5%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Sports and Recreations 1 5%
Other 1 5%
Unknown 7 32%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 May 2018.
All research outputs
#7,717,825
of 25,382,440 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#470
of 2,382 outputs
Outputs of similar age
#124,640
of 343,066 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#14
of 39 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one has received more attention than most of these and is in the 69th percentile.
So far Altmetric has tracked 2,382 research outputs from this source. They receive a mean Attention Score of 4.8. This one has done well, scoring higher than 79% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 343,066 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 63% of its contemporaries.
We're also able to compare this research output to 39 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 64% of its contemporaries.