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Record W2801195276 · doi:10.1093/cvr/cvy060.162

231Myocardin regulates mitochondrial calcium homeostasis and prevents permeability transition in cardiac myocytes

2018· article· en· W2801195276 on OpenAlexaffabout
Wajihah Mughal, Matthew D. Martens, Jared T. Field, Donald Chapman, Richard Keijzer, Sunil G. Rattan, Ian Dixon, Jiang Rong Huang, Michael S. Parmacek, Joseph W. Gordon

Bibliographic record

VenueCardiovascular Research · 2018
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicMitochondrial Function and Pathology
Canadian institutionsUniversity of Manitoba
FundersSydäntutkimussäätiöNational Cerebral and Cardiovascular CenterSuomen Lääketieteen Säätiö
KeywordsMitochondrial permeability transition poreHomeostasisMyocyteCalciumMitochondrionCell biologyCalcium metabolismInternal medicineEndocrinologyCalcium signalingCardiac myocyteChemistryBiologyMedicineBiochemistryApoptosisProgrammed cell death

Abstract

fetched live from OpenAlex

Funding Acknowledgements: Research Manitoba, Natural Sciences & Engineering Council of Canada, Diabetes Research Envisioned and Accomplished in Manitoba Myocardin is a transcriptional co-activator required for cardiovascular development and cardiomyocyte differentiation. Recent studies have shown that genetic inhibition of myocardin results in embryonic lethality with impaired cardiomyocyte proliferation and increased programmed cell death. Mitochondrial permeability transition, triggered by matrix calcium accumulation, has been implicated in regulated necrotic cell death, while permeability transition pore closure is involved with myocyte differentiation and mitochondrial maturation during development. We show that a genetic loss of myocardin function leads to endocardial necrosis, determined by HMGB1 staining, at embryonic day 9.5, concurrent with elevated expression of the death gene Nix. Mechanistically, we demonstrate that myocardin knockdown in primary ventricular myocytes reduces microRNA-133a levels to allow Nix accumulation, leading to mitochondrial permeability transition, reduced mitochondrial respiration, and necrosis. Using organelle-targeted calcium biosensors, we demonstrate that myocardin knockdown leads to sarcoplasmic reticulum (SR) calcium release and mitochondrial calcium accumulation, while mitochondrial permeability transition was prevented by pharmacological inhibition of the inositol triphosphate (IP3)-activated calcium channel or the mitochondrial calcium uniporter. Gain of function studies confirm that myocardin can desensitize myocytes to permeability transition elicited by protein kinase-A (PKA) activating agents by opposing SR calcium release. Furthermore, restoring microRNA-133a function with mimicking oligonucleotides, or knockdown of Nix rescues mitochondrial calcium accumulation induced by myocardin knockdown. Molecular studies using Nix constructs targeted to the SR or mitochondria revealed that only SR-targeted Nix leads to mitochondrial calcium accumulation, which could be attenuated by SR-targeted Bcl-2, but not mitochondrial-targeted Bcl-2. Finally, we observed reduced myocardin expression in vivo within the infarction border zone following coronary ligation in rodents, with corresponding reduced microRNA-133a and elevated Nix expression. These findings identify a novel myocardin-regulated genetic pathway that maintains cardiomyocyte calcium homeostasis and mitochondrial function during development, and is attenuated during ischemic heart disease.

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)0.002
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 score0.289
Threshold uncertainty score0.785

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0020.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.001
Bibliometrics0.0000.000
Science and technology studies0.0000.001
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 head0.043
GPT teacher head0.322
Teacher spread0.278 · 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".

Quick stats

Citations1
Published2018
Admission routes2
Has abstractyes

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