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Record W4410645236 · doi:10.1007/s10456-025-09982-8

Human endothelial colony forming cells (ECFCs) require endothelial protein C receptor (EPCR) for cell cycle progression and angiogenic activity

2025· article· en· W4410645236 on OpenAlexfundno aff
Sarah Chambers, Jasenka Guduric‐Fuchs, Edoardo Pedrini, Pietro Maria Bertelli, Chutima Charoensuk, Elisa Peixoto, Varun Pathak, Ruoxiao Xie, Anna Krasnodembskaya, Judith Lechner, Alan W. Stitt, Reinhold J. Medina

Bibliographic record

VenueAngiogenesis · 2025
Typearticle
Languageen
FieldMedicine
TopicBlood Coagulation and Thrombosis Mechanisms
Canadian institutionsnot available
FundersBiotechnology and Biological Sciences Research CouncilQueen's UniversityQueen's University BelfastMedical Research CouncilDunhill Medical TrustDiabetes UKMacular SocietyLeverhulme TrustDepartment for the EconomyWellcome Trust
KeywordsEndothelial protein C receptorCell biologyAngiogenesisBiologyGene knockdownStem cellCancer researchCell cycleCell growthProgenitor cellCellImmunologyCell cultureThrombin

Abstract

fetched live from OpenAlex

Vascular repair and regeneration are critical for tissue homeostasis. Endothelial colony forming cells (ECFCs) are vessel-resident progenitors with vasoreparative capacity and they offer an important avenue for allogeneic cytotherapy to achieve perfusion of ischemic tissues. Endothelial Protein C Receptor (EPCR) has been proposed as a marker for vascular endothelial stem cells, but its precise role in ECFC biology remains unknown. The current study has investigated the biological relevance of EPCR in ECFC function. Our data show that over 95% of ECFCs exhibit high EPCR expression. These levels surpassing CD34 and CD157, positions EPCR as a new robust ECFC immunophenotypic marker, alongside established markers CD31 and CD105. Functionally, depleting EPCR expression in ECFCs significantly diminished angiogenic activity, including proliferation, migration and tube formation. This knockdown also altered normal ECFC barrier function. Transcriptomic analysis indicated that knockdown of EPCR led to enrichment of gene signatures for cell cycle, TGF beta, and focal adhesion kinases. G1 cell cycle arrest was confirmed in ECFCs with depleted EPCR. Mechanistically, EPCR knockdown led to increased release of TGFβ2 and SMAD2/3 activation, coupled with increased p21, decreased pFAK, and increased transgelin. Additionally, we showed that quiescent ECFCs showed significantly lower EPCR expression when compared to proliferating ECFCs. In agreement with this, cell sorting experiments demonstrated that ECFCs with the highest EPCR expression exhibited the highest clonogenic capacity. In summary, our findings highlight that EPCR expression in ECFCs is critical for their angiogenic activity, by modulating cell cycle progression.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.021
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.018
GPT teacher head0.298
Teacher spread0.280 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations4
Published2025
Admission routes1
Has abstractyes

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