miR‐141 inhibition protects cardiomyocytes from anoxia/reoxygenation‐induced mitochondrial dysfunction
Bibliographic record
Abstract
Background Mitochondrial dysfunction plays an important role in ischemia/reperfusion (I/R) ‐induced myocardial injury. MicroRNAs are involved in myocardial injury after I/R. It has been reported that miR‐141 contributes to mitochondrial dysfunction in mice with diabetes. The aim of the present study is to dertmine whether the miR‐141 contributes to I/R‐induced myocardial injury and the underlying mechanism. Methods HL‐1 cells were challenged with an anoxia/reoxygenation (A/R). miR‐141 expression in HL‐1 cells was detected by qRT‐PCR. Mitofusin‐2 (Mfn2) was assessed with Western blot. HL‐1 cellular oxygen consumption rate (OCR) was assessed with Seahorse XF24 analyzer. Results A/R challenge to HL‐1 cells increased miR‐141 expression and peaked at 12 hours after the reoxygenation. A/R challenge resulted in decreased mitochondrial membrane potential, OCR and ATP production of the cardiomyocytes, as well as increased LDH activity in the supernatant of the cardiomyocytes. The above changes were attenuated by transfection of the cardiomyocytes with miR‐141 inhibitor before the A/R. Overexpression of miR‐141 in the HL‐1 cell exaggerated the A/R‐induced mitochondrial dysfunction and cardiomyocyte injury. The A/R challenge to HL‐1 cells led to a decreased Mfn2 expression. Transfection of HL‐1 cells with miR‐141 mimics suppressed Mfn2 expression. Conclusion Our data indicate that miR‐141 is involved in A/R‐induced mitochondrial dysfunction by modulating Mfn2 protein expression. Support or Funding Information The study was supported by Natural Science Foundation of Jiangsu Province (BK20151332) and Natural Science Foundation of China (81370333). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot 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.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
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.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
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".