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Record W2295248503 · doi:10.1161/atvb.35.suppl_1.38

Abstract 38: Cyclin-Dependent Kinase Inhibitor 2B Regulates Transforming Growth Factor Beta 1 Mediated Smooth Muscle Cell Recruitment to Ischemic Blood Vessels

2015· article· en· W2295248503 on OpenAlexaff
Vivek Nanda, Kelly Downing, Yoko Kojima, Jessie Dalman, Daniel DiRenzo, Andrew J. Connolly, Lars Mäegdefessel, Ljubica Perisic, Sonny Dandona, Liang Guo, Harry R. Davis, Renu Virmani, Joshua M. Spin, Nicholas J. Leeper

Bibliographic record

VenueArteriosclerosis Thrombosis and Vascular Biology · 2015
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicAngiogenesis and VEGF in Cancer
Canadian institutionsMcGill University
Fundersnot available
KeywordsBiologyAlleleCancer researchTransforming growth factor betaAngiogenesisGenome-wide association studySMADTransforming growth factorPathologyCell biologyMedicineGeneticsGenotypeSingle-nucleotide polymorphismGene

Abstract

fetched live from OpenAlex

Peripheral artery disease (PAD) is a highly morbid condition affecting nearly 8.5 million Americans. Genome wide association studies (GWAS) have identified genetic variation at the chromosome 9p21 cardiovascular risk locus as an important source of heritable PAD risk. However, it is unknown whether this association is secondary to an increase in atherosclerosis or is the result of a separate angiogenesis-related mechanism. Quantitative ultrastructural evaluation of human plaque laden vascular samples revealed that carriers of the 9p21 risk allele displayed a significantly increased burden of immature intraplaque microvessels than carriers of the ancestral allele. To determine whether this process occurs under non-atherosclerotic conditions, we performed femoral artery ligation surgery in mice lacking Cdkn2b; a candidate gene we previously identified to have reduced expression in human carriers of the 9p21 risk allele. These animals developed advanced hind-limb ischemia and digital auto-amputation, relative to wild-type controls. Interestingly, in situ and in vitro hypoxic assays identified this defect to be a consequence of pro-angiogenic behavior displayed by CDKN2B deficient endothelial cells (EC) and impaired smooth muscle cell (SMC) recruitment to the developing neovessel. Exploratory microarray studies performed to identify the mechanism involved, revealed that TGFβ1 signaling is significantly induced in cultured CDKN2B -deficient cells; a finding later confirmed in the vasculature of individuals carrying the 9p21 risk allele. Subsequent molecular signaling studies reveal this increase to be a result of impaired expression of the inhibitory factor, SMAD-7. Increased TGFβ1 signaling was ultimately found to manifest the upregulation of a poorly studied effector molecule, TGFβ1-induced-1, which is a TGFβ-‘rheostat’ known to have antagonistic effects on the EC and SMC. Dual knockdown and rescue studies confirmed the reversibility of the proposed mechanism, in vitro. Taken together these findings suggest that loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis, but may also impair TGFβ1 signaling and hypoxic neovessel maturation consequently resulting in PAD.

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 machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
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 score0.004
Threshold uncertainty score0.014

Distilled classifier scores by category (both heads)

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)0.0040.001

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 head0.052
GPT teacher head0.283
Teacher spread0.232 · 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 source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
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

Citations0
Published2015
Admission routes1
Has abstractyes

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