Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts
Bibliographic record
Abstract
This study aimed to explore the potential contribution of myofibrils to contractile dysfunction in Ca 2+ -paradox hearts. Isolated rat hearts were perfused with Krebs–Henseleit solution (Control), followed by Ca 2+ -depletion, and then Ca 2+ -repletion after Ca 2+ -depletion (Ca 2+ -paradox) by Langendorff method. During heart perfusion left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of pressure development (+ dP/dt), and pressure decay (-dP/dt) were registered. Control LVDP (127.4 ± 6.1 mmHg) was reduced during Ca 2+ -depletion (9.8 ± 1.3 mmHg) and Ca 2+ -paradox (12.9 ± 1.3 mmHg) with similar decline in +dP/dt and –dP/dt. LVEDP was increased in both Ca 2+ -depletion and Ca 2+ -paradox. Compared to Control, myofibrillar Ca 2+ -stimulated ATPase activity was decreased in the Ca 2+ -depletion group (12.08 ± 0.57 vs. 8.13 ± 0.19 µmol P i /mg protein/h), besides unvarying Mg 2+ ATPase activity, while upon Ca 2+ -paradox myofibrillar Ca 2+ -stimulated ATPase activity was decreased (12.08 ± 0.57 vs. 8.40 ± 0.22 µmol P i /mg protein/h), but Mg 2+ ATPase activity was increased (3.20 ± 0.25 vs. 7.21 ± 0.36 µmol P i /mg protein/h). In force measurements of isolated cardiomyocytes at saturating [Ca 2+ ], Ca 2+ -depleted cells had lower rate constant of force redevelopment ( k tr,max , 3.85 ± 0.21) and unchanged active tension, while those in Ca 2+ -paradox produced lower active tension (12.12 ± 3.19 kN/m 2 ) and k tr,max (3.21 ± 23) than cells of Control group (25.07 ± 3.51 and 4.61 ± 22 kN/m 2 , respectively). In biochemical assays, α-myosin heavy chain and cardiac troponin T presented progressive degradation during Ca 2+ -depletion and Ca 2+ -paradox. Our results suggest that contractile impairment in Ca 2+ -paradox partially resides in deranged sarcomeric function and compromised myofibrillar ATPase activity as a result of myofilament protein degradation, such as α-myosin heavy chain and cardiac troponin T. Impaired relaxation seen in Ca 2+ -paradoxical hearts is apparently not related to titin, rather explained by the altered myofibrillar ATPase activity.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot 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.
Codex and Gemma teacher scores by category
| 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 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 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 teacher head, 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".