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Changes in gene expression caused by genetic elimination of high molecular weight FGF2 are associated with prevention of stress‐induced cardiac systolic dysfunction

2020· article· en· W3016577620 on OpenAlexaffabout
Elissavet Kardami, Navid Koleini, Barbara E. Nickel, Raghu S. Nagalingam, Natalie M. Landry, Robert R. Fandrich, David Cheung, Ian Dixon, Michael P. Czubryt, Davinder S. Jassal, Peter A. Cattini

Bibliographic record

VenueThe FASEB Journal · 2020
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicFibroblast Growth Factor Research
Canadian institutionsUniversity of Manitoba
Fundersnot available
KeywordsEndocrinologyInternal medicineEndogenyPressure overloadFibroblast growth factorCardiac function curveMicroarray analysis techniquesHsp70Circadian rhythmGene expressionMedicineHeat shock proteinBiologyReceptorGeneMuscle hypertrophyHeart failureBiochemistry

Abstract

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Fibroblast growth factor 2 (FGF2) is produced as high (>20 kDa, Hi‐) and low molecular weight (18 kDa, Lo) isoforms in the heart. While administered Lo‐FGF2 has been established as a cardioprotective agent in multiple models of cardiac injury, there is limited information about the role of Hi‐FGF2 in the heart. To investigate the effect of endogenous Hi‐FGF2 we compared cardiac transcriptome (35240 targets, GeneChip™ Mouse Gene 2.0 ST Array (Affymetrix, 902119)) and systolic function between Hi‐FGF2 knock‐out mice, FGF2(Lo), expressing only Lo‐FGF2, and wild type mice, FGF2(WT), expressing both Hi‐FGF2 and Lo‐FGF2, under ‘normal’ (sham‐operated) and “stress” (pressure overload) conditions. Transaortic constriction surgery (TAC) was used to induce pressure overload. Echocardiography was done at baseline and at 4–8 weeks post‐surgery. Microarray analysis showed that under normal conditions, the absence of Hi‐FGF2 promoted changes in relative levels of 118 transcripts, including those associated with circadian rhythm regulation and heat shock protein (HSP70)‐associated apoptosis regulation. Comparative analysis of TAC surgery‐induced gene expression changes showed that 275 transcripts were differentially affected by the presence or absence of Hi‐FGF2 expression, most prominently the orphan nuclear receptor NR1D1 which is linked to regulation of circadian rhythm and metabolism. Under non‐stress conditions, systolic function was unaffected by endogenous Hi‐FGF2 expression. Pressure overload stress caused a decline in systolic function in the presence of endogenous Hi‐FGF2, at 4–8 weeks post‐TAC surgery, accompanied by increases in markers of myocardial stress/damage including B‐type natriuretic peptide (BNP) and the pro‐cell death protein BCL2/adenovirus E1B 19 kDa protein‐interacting protein‐3, Bnip3. In the absence of endogenous Hi‐FGF2, mice were protected from stress‐induced loss of systolic function and increases in BNP and Bnip3. TAC surgery induced Hi‐FGF2‐independent increases in: cardiac mass (heart weight/tibia length); cardiac fibrosis; transcripts linked to exracellular matrix remodeling. Increased cardiomyocyte size, however, was only observed in FGF2(WT) but not FGF2(Lo) hearts post‐TAC. It is suggested that elimination of endogenous Hi‐FGF2 elicits cardioprotection by increasing cardiac HSP70 (pre‐TAC surgery); and NR1D1, after TAC surgery. Support or Funding Information Funding (EK, PAC, DJ) was provided by the Canadian Institutes for Health Research (FRN‐74733) and the Molson Women’s Heart Health Foundation (EK). MPC was supported by a CIHR Open Operating Grant (MOP136862). NK and RSN were the recipients of a Bank of Montreal studentship award via the St. Boniface Hospital Albrechtsen Research Centre and University of Manitoba funding to PAC.

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 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 score0.041
Threshold uncertainty score0.384

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 head0.013
GPT teacher head0.235
Teacher spread0.222 · 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.

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".

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Citations2
Published2020
Admission routes2
Has abstractyes

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