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Myocardin Regulated Genetic Pathway Modulates Mitochondrial Permeability Transition Pore Closure to Prevent Cell Death during Cardiac Differentiation

2016· article· en· W2588873883 on OpenAlexafffundabout
Wajihah Mughal, Simone da Silva Rosa, Yang Hai, William Diehl‐Jones, Joseph W. Gordon

Bibliographic record

VenueThe FASEB Journal · 2016
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicMitochondrial Function and Pathology
Canadian institutionsAthabasca UniversityUniversity of Manitoba
FundersChildren’s Hospital Foundation of Manitoba
KeywordsMitochondrial permeability transition poreMyocardinCell biologyMitochondrial DNAChemistryClosure (psychology)Programmed cell deathBiologyApoptosisTranscription factorBiochemistryGeneSerum response factor

Abstract

fetched live from OpenAlex

Myocardin is a transcriptional co‐activator required for cardiovascular development and cardiomyocyte differentiation. Recent studies have shown that genetic inhibition of myocardin results in congenital heart defects associated with increased programmed cell death (PCD). In addition to its established role in regulating PCD, the mitochondrial permeability transition pore (PTP) has been implicated in cardiac calcium homeostasis and myocyte maturation during development. Utilizing fluorescent staining and biochemical assays, we demonstrate that myocardin, a modulator of cardiac gene function, regulates mitochondrial PTP closure during myocyte differentiation to oppose pathways of PCD induced by protein kinase‐A (PKA) activating agents. We show that a loss of myocardin function reduces microRNA‐133a (miR‐133a) mRNA levels and induces mitochondrial dysfunction by PTP opening and reducing mitochondrial membrane potential. Furthermore, myocardin knockdown increased mitochondrial oxidative stress and mitochondrial calcium uptake in differentiated myocytes. Conversely, restoring myocardin expression rescued mitochondrial function, concurrent with a decreased expression of a mitochondrial death protein, Nix. Furthermore, miR‐133a protects against PKA‐activating agents while inhibitory molecules opposing miR‐133a increase Nix expression. With the use of genetically encoded and organelle targeted calcium sensors, our data demonstrates that miR‐133a reverses endoplasmic reticulum calcium release and prevents mitochondrial calcium uptake, in a manner dependent on Nix repression. Finally, we provide mechanistic evidence that myocardin‐dependent miR‐133a expression is regulated by histone deactylase‐5 (HDAC5) and the PKA‐regulated salt inducible kinase‐1 (SIK1). These findings support the notion that myocardin opposes PCD through mitochondrial permeability transition by regulating calcium homeostasis; however, this genetic pathway may be attenuated by pathological PKA signaling. Support or Funding Information Supported by Children's Hospital Foundation of Manitoba, Research Manitoba and NSERC Canada.

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 score0.001
Threshold uncertainty score0.004

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 integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

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 head0.008
GPT teacher head0.206
Teacher spread0.198 · 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
Published2016
Admission routes3
Has abstractyes

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