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Record W4323538068 · doi:10.1101/2023.03.06.531384

MK2 deficiency decreases mortality during the inflammatory phase after myocardial infarction in mice

2023· preprint· en· W4323538068 on OpenAlexafffund
Joëlle Trépanier, Sherin A. Nawaito, Pramod Sahadevan, Fatiha Sahmi, Natacha Duquette, Danielle Gélinas, Marc‐Antoine Gillis, Yanfen Shi, Cynthia Torok, Marie‐Élaine Clavet‐Lanthier, Matthias Gaestel, Martin G. Sirois, Jean‐Claude Tardif, Bruce G. Allen

Bibliographic record

VenuebioRxiv (Cold Spring Harbor Laboratory) · 2023
Typepreprint
Languageen
FieldMedicine
TopicCardiac Fibrosis and Remodeling
Canadian institutionsUniversité de MontréalMontreal Heart Institute
FundersInstitut de Cardiologie de MontréalHeart and Stroke Foundation of CanadaFondation Institut de Cardiologie de MontréalUniversité de MontréalPfizer
KeywordsMedicineMyocardial infarctionInternal medicineCardiologyLigationInflammationChemokineEndocrinology

Abstract

fetched live from OpenAlex

Abstract Background: Altering the onset, intensity, or duration of inflammation can impact the recovering heart’s structure and function following myocardial infarction (MI). Substrates of MAP kinase-activated protein kinase 2 (MK2) include proteins that regulate the stability of AU-rich transcripts, including those of several pro-inflammatory cytokines. This study was to determine if MK2-deficiency impaired the inflammatory phase of post-MI wound repair. Methods and Results: Myocardial infarctions were induced by permanent ligation of the left anterior descending coronary artery in 12-week-old male MK2 +/+ and MK2 -/- littermate mice. Five days post-MI, survival was 100% in MI-MK2 -/- (n = 20) and 79% in MI-MK2 +/+ mice (n = 29; Mandel-Cox test: P < 0.05). Area at risk and infarct size were similar. Echocardiographic imaging revealed that both systolic and diastolic LV diameters were greater in MI-MK2 +/+ than MI-MK2 -/- mice. MK2-deficiency did not affect the increase in wall motion score index. Infiltration of neutrophils or monocytes did not differ significantly. Cytokine and chemokine transcripts were quantified in infarcted and non-infarcted LV tissue using qPCR arrays (QIAGEN). Three days post-MI, Ifna2 was increased and Il16 was decreased in infarcted tissue from MK2 -/- hearts, compared with infarcted MK2 +/+ tissue, whereas in the non-infarcted MK2 -/- myocardium Il27 increased and Tnfsf11 , Ccl3 , and Il1rn were decreased. Five days post-MI, Ctf16 and Il10 increased in infarcted MK2 -/- tissue whereas in the non-infarcted MK2 -/- myocardium Ccl9, Nodal, and Xcl2 increased and Il15 decreased. Conclusions: The findings of this study suggest MK2-deficiency is an advantage during the inflammatory phase of cardiac wound repair post-MI. Clinical Perspective What is new? -The effects of MAP kinase-activated protein kinase 2 (MK2) deficiency on survival, cardiac structure and function, and the inflammatory phase of wound healing following myocardial infarction were assessed using a constitutive, pan MK2-null mouse model. -MK2-deficiency reduced mortality but did not alter area at risk or infarct size post-myocardial infarction. Inflammatory cell infiltration was also unaffected. -MK2-deficiency altered the abundance of several cytokines (increased, decreased) in infarcted and non-infarcted myocardium post-MI. What are the clinical implications? -The initial phase of wound repair post-MI involves inflammation. -The risk of damage to the myocardium and mortality may be reduced by inhibition of MK2 activity during the inflammatory phase of wound healing post-MI.

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)0.001
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: Observational · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.624
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0010.001
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.001
Research integrity0.0010.001
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 head0.260
Teacher spread0.241 · 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 designObservational
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
Published2023
Admission routes2
Has abstractyes

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