MétaCan
Menu
← Back to cohort

Sarcolipin Deletion in <i>mdx</i> Mice Worsens Dystrophic Pathology by Impairing Calcineurin Signaling and Reducing Utrophin Expression

2016· article· en· W4389007859 on OpenAlexafffundabout
Val A. Fajardo, Daniel Gamu, Bradley A Rietze, Frenk Kwon, Paige J. Chambers, Joe Quadrilatero, A. Russell Tupling

Bibliographic record

VenueThe FASEB Journal · 2016
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicMuscle Physiology and Disorders
Canadian institutionsUniversity of Waterloo
FundersCanadian Institutes of Health Research
KeywordsUtrophinmdx mouseDystrophinDuchenne muscular dystrophyCalcineurinMuscular dystrophyKnockout mouseEndocrinologyInternal medicineBiologyMedicineCell biologyTransplantationReceptor

Abstract

fetched live from OpenAlex

Duchenne's muscular dystrophy (DMD) is the most severe form of muscular dystrophy affecting 1 in 3500 live male births. There is no cure for DMD and males typically succumb to early mortality induced by respiratory and cardiac insufficiency. Thus, finding viable therapeutic targets is of utmost importance. Sarcolipin (SLN), a sarco(endo)plasmic reticulum Ca 2+ ‐ATPase (SERCA) pump inhibitor, is highly upregulated in dystrophic muscles from mdx mice, a mouse model for DMD. To date, the role of SLN in muscular dystrophy remains unknown, and therefore, in this study we crossed Sln KO mice with mdx mice to generate the mdx / Sln KO double knockout mutant mouse. We hypothesized that Sln deletion would worsen dystrophic myopathy based on unpublished results from our laboratory and previous studies showing that SLN can stimulate calcineurin – a Ca 2+ ‐dependent serine/threonine phosphatase shown to counteract muscular dystrophy. Our findings show that mdx / Sln KO myofibers from soleus ( P = 0.0001) and diaphragm ( P < 0.0001) were significantly smaller than those from mdx . Furthermore, mdx / Sln KO soleus and diaphragm muscles displayed a slow‐to‐fast fiber type shift, which was associated with a significant reduction in utrophin ( P = 0.004). Utrophin, a dystrophin homolog that confers compensatory membrane stability, is largely controlled by calcineurin, suggesting that SLN in mdx mice stimulates calcineurin signaling. In addition, the significant reductions in utrophin expression in the mdx / Sln KO mice can account for their worsened dystrophic pathology revealed by greater serum creatine kinase ( P = 0.01) and greater variability in myofiber size (minimal Feret's diameter, P = 0.01) compared with mdx . Finally, lower central nuclei counts in muscles from mdx / Sln KO mice compared with mdx ( P = 0.04) suggests that genetic deletion of Sln also potentially impairs the muscles’ regenerative capacity. Taken together, these results, for the first time clearly demonstrate SLN's vital role in countering muscular dystrophy. Support or Funding Information This work was supported by the Canadian Institutes of Health Research (CIHR; MOP 86618 and MOP 47296 to A.R.T).

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 score0.004
Threshold uncertainty score0.012

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0010.000
Science and technology studies0.0000.001
Scholarly communication0.0010.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0040.001

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 head0.006
GPT teacher head0.222
Teacher spread0.215 · 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

Citations1
Published2016
Admission routes3
Has abstractyes

Explore more

Same venueThe FASEB Journal→Same topicMuscle Physiology and Disorders→French-language works237,207→