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 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) | 0.001 | 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 | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 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".