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Abstract 20130: Hypertrophic Cardiomyopathy in RAF1 Mutant-associated Noonan Syndrome Requires Complex Cellular Interplay

2015· article· en· W2341214674 on OpenAlexaff
Jiani C. Yin, Mathew J. Platt, Xue Wu, Jeremy A. Simpson, Toshiyuki Araki, Benjamin G. Neel

Bibliographic record

VenueCirculation · 2015
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicProtein Tyrosine Phosphatases
Canadian institutionsUniversity of GuelphUniversity of Toronto
Fundersnot available
KeywordsPressure overloadMedicineHypertrophic cardiomyopathyContractilityMuscle hypertrophyInternal medicineEndocrinologyCancer researchCell biologyBiology

Abstract

fetched live from OpenAlex

Hypertrophic cardiomyopathy (HCM) has multiple etiologies, including hypertension, cardiac valve disease or genetic defects. Most inherited HCM results from defects in sarcomere proteins, but ~25% are caused by aberrant cardiac signal transduction genes. RASopathies are developmental disorders with multiple variably penetrant features, including HCM, which are caused by mutations in genes encoding RAS/extracellular signal-regulated kinase (ERK) pathway components. The most common RASopathy, Noonan Syndrome (NS), results from gain-of-function alleles in PTPN11, KRAS, SHOC2, SOS1/2, RAF1 and RIT1. Activating mutations in RAF1 are strongly (~95%) associated with HCM. Global knock-in mice harboring the NS allele Raf1L613V recapitulate the features of NS-associated HCM, including ventricular chamber dilatation, enhanced cardiac contractility, and exacerbation of pressure-overload induced fibrosis. Here, using inducible Raf1L613V knock-in mice and lineage-specific Cre lines, we show that RAF1 mutant-associated HCM is caused by a complex interplay of multiple cardiac cell types. Surprisingly, cardiomyocyte-specific Raf1L613V expression caused minimal hypertrophy, yet markedly increased cardiac contractility. By contrast, endocardial/cardiac endothelial (EC)-specific Raf1L613V expression promoted cardiomyocyte hypertrophy without affecting contractility. In direct or Transwell co-cultures, Raf1L613V-expressing ECs increased the size of normal cardiomyocytes. Cytokine arrays revealed increased IL6 secretion from isolated Raf1L613V-expressing ECs, and JAK-STAT, PI3K, and MEK/ERK activation were enhanced in EC-Raf1L613V hearts. Blocking IL6 action with neutralizing anti-IL6 antibodies reversed cardiomyocyte hypertrophy in EC/cardiomyocyte co-cultures. Finally, Raf1L613V expression in cardiomyocytes or cardiac fibroblasts, but not in ECs, exacerbated fibrosis upon pressure-overload. Taken together, our data indicate that NS HCM requires complex, cell-autonomous and -non-autonomous interactions between cardiomyocytes, ECs, and fibroblasts. Furthermore, we identify the IL6 pathway as a potential therapeutic target for RASopathy-associated HCM.

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 score0.006
Threshold uncertainty score0.020

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 integrity0.0010.001
Insufficient payload (model declined to judge)0.0060.002

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 head0.028
GPT teacher head0.260
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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