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Analysis of institutional authors

Barroso SAuthorCaballero áAuthorRibas CAuthorCorreas IAuthorMillan JAuthor
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Article

Compensatory increase of VE-cadherin expression through ETS1 regulates endothelial barrier function in response to TNFα

Publicated to:CELLULAR AND MOLECULAR LIFE SCIENCES. 77 (11): 2125-2140 - 2020-06-01 77(11), DOI: 10.1007/s00018-019-03260-9

Authors: Colas-Algora, Natalia; Garcia-Weber, Diego; Cacho-Navas, Cristina; Barroso, Susana; Caballero, Alvaro; Ribas, Catalina; Correas, Isabel; Millan, Jaime

Affiliations

CSIC-UAM - Centro de Biología Molecular Severo Ochoa (CBM) - Author
INSERM, U1016, Inst Cochin, Paris, France - Author
Inst Invest Sanitaria Princesa, Madrid 28006, Spain - Author
Institut Cochin - Author
Instituto de Investigacion Sanitaria La Fe - Author
Instituto de Salud Carlos III - Author
ISCIII CIBERCV, CIBER Enfermedades Cardiovasc, Madrid 28029, Spain - Author
UAM, Ctr Biol Mol Severo Ochoa, CSIC, Madrid 28049, Spain - Author
Univ Autonoma Madrid, Dept Biol Mol, Madrid 28049, Spain - Author
Universidad Autónoma de Madrid - Author
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Abstract

© 2019, Springer Nature Switzerland AG. VE-cadherin plays a central role in controlling endothelial barrier function, which is transiently disrupted by proinflammatory cytokines such as tumor necrosis factor (TNFα). Here we show that human endothelial cells compensate VE-cadherin degradation in response to TNFα by inducing VE-cadherin de novo synthesis. This compensation increases adherens junction turnover but maintains surface VE-cadherin levels constant. NF-κB inhibition strongly reduced VE-cadherin expression and provoked endothelial barrier collapse. Bacterial lipopolysaccharide and TNFα upregulated the transcription factor ETS1, in vivo and in vitro, in an NF-κB dependent manner. ETS1 gene silencing specifically reduced VE-cadherin protein expression in response to TNFα and exacerbated TNFα-induced barrier disruption. We propose that TNFα induces not only the expression of genes involved in increasing permeability to small molecules and immune cells, but also a homeostatic transcriptional program in which NF-κB- and ETS1-regulated VE-cadherin expression prevents the irreversible damage of endothelial barriers.

Keywords
adherens junctionsdegradationendothelial barrier functionets1lpsnf-?bnf-κbpermeabilityresolution of inflammationActivationAdherens junctionsAdhesionAnimalsAntigens, cdCadherin 5CadherinsCapillary permeabilityCellsDegradationEndothelial barrier functionEndothelial cellsEts1Ets1 protein, humanGene silencingHuman umbilical vein endothelial cellsHumansInflammationLpsMembraneMiceNecrosis-factor-alphaNf-?bNf-kappa bNf-κbPermeabilityProteinProteolysisProto-oncogene protein c-ets-1Resolution of inflammationTranscription factor ets-1Tumor necrosis factor-alphaTyrosine phosphorylationUp-regulationVe-cadherin

Quality index

Bibliometric impact. Analysis of the contribution and dissemination channel

The work has been published in the journal CELLULAR AND MOLECULAR LIFE SCIENCES due to its progression and the good impact it has achieved in recent years, according to the agency WoS (JCR), it has become a reference in its field. In the year of publication of the work, 2020, it was in position 30/298, thus managing to position itself as a Q1 (Primer Cuartil), in the category Biochemistry & Molecular Biology. Notably, the journal is positioned above the 90th percentile.

From a relative perspective, and based on the normalized impact indicator calculated from World Citations provided by WoS (ESI, Clarivate), it yields a value for the citation normalization relative to the expected citation rate of: 1.06. This indicates that, compared to works in the same discipline and in the same year of publication, it ranks as a work cited above average. (source consulted: ESI Nov 14, 2024)

This information is reinforced by other indicators of the same type, which, although dynamic over time and dependent on the set of average global citations at the time of their calculation, consistently position the work at some point among the top 50% most cited in its field:

  • Field Citation Ratio (FCR) from Dimensions: 4.04 (source consulted: Dimensions Apr 2025)

Specifically, and according to different indexing agencies, this work has accumulated citations as of 2025-04-30, the following number of citations:

  • WoS: 20
  • Scopus: 20
  • Europe PMC: 14
  • OpenCitations: 37
Impact and social visibility

From the perspective of influence or social adoption, and based on metrics associated with mentions and interactions provided by agencies specializing in calculating the so-called "Alternative or Social Metrics," we can highlight as of 2025-04-30:

  • The use, from an academic perspective evidenced by the Altmetric agency indicator referring to aggregations made by the personal bibliographic manager Mendeley, gives us a total of: 45.
  • The use of this contribution in bookmarks, code forks, additions to favorite lists for recurrent reading, as well as general views, indicates that someone is using the publication as a basis for their current work. This may be a notable indicator of future more formal and academic citations. This claim is supported by the result of the "Capture" indicator, which yields a total of: 45 (PlumX).

With a more dissemination-oriented intent and targeting more general audiences, we can observe other more global scores such as:

  • The Total Score from Altmetric: 1.
  • The number of mentions on the social network X (formerly Twitter): 1 (Altmetric).

It is essential to present evidence supporting full alignment with institutional principles and guidelines on Open Science and the Conservation and Dissemination of Intellectual Heritage. A clear example of this is:

  • The work has been submitted to a journal whose editorial policy allows open Open Access publication.
Leadership analysis of institutional authors

This work has been carried out with international collaboration, specifically with researchers from: France.

There is a significant leadership presence as some of the institution’s authors appear as the first or last signer, detailed as follows: First Author (Colás-Algora N) and Last Author (MILLAN MARTINEZ, JAIME).