Angiotensin‐II‐induced expression of the early growth response protein 1 is mediated by CaMKII‐dependent pathway in vascular smooth muscle cells (1011.7)
Bibliographic record
Abstract
Egr‐1 is a transcription factor implicated in the regulation of several growth‐related cascades. It has been suggested to participate in the development of vascular disease processes such as intimal thickening following vascular injury, atherosclerosis and cardiac hypertrophy. Upregulation of Egr‐1 was recently shown to be a key contributing factor in stimuli‐induced VSMC proliferation and hypertrophy. Ang‐II, a potent vasoactive peptide with pathogenic role in vascular disease, has been demonstrated to contribute to aberrant remodeling of the vessel wall. This is mainly due to the ability of Ang‐II to activate hypertrophic and proliferative pathways such as the mitogen‐activated protein kinase and the phosphatidylinositol‐3‐kinase pathways in VSMC. It has been shown earlier that Ang‐II requires H 2 O 2 generation to activate these signaling pathways and we have shown that Ca 2+ , calmodulin (CaM) and Ca 2+ /CaM‐dependent protein kinase II(CaMKII), play a critical role to trigger H2O2‐induced effects in VSMC. We have also shown that endothelin‐1, another mitogenic vasoactive peptide, requires CaMKII to upregulate Egr‐1 expression and to mediate its physiological responses. However, Ang‐II‐induced modulation of Egr‐1 expression in VSMC and the implication of CaMKII in this process remain unexplored. Therefore these studies were undertaken to characterize the effect of Ang‐II on Egr‐1 expression in A10 VSMC and to examine the role of Ca 2+ , CaM and CaMKII on this response. Ang‐II, at 100nM, induced an increase in Egr‐1 expression in a time‐dependent fashion in the nucleus of A10 VSMC. Pharmacological blockade of CaM and CaMKII by calmidazolium and KN‐93 respectively, significantly attenuated Ang‐II‐induced Egr‐1 expression. These results demonstrate that Egr‐1 expression is upregulated in response to Ang‐II via CaM/CaMKII‐dependent pathways in VSMC. Grant Funding Source : Supported by the Canadian Institutes of Health Research
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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) | 0.000 | 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) | 0.001 | 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".