Apoptosis in hypoxic mice influenced by miR-138-siRNAs-HIF-1α and miR- 21-siRNAs-HVCN1
Bibliographic record
Abstract
Abstract Background The complications of intraventricular-cerebral hemorrhage in premature infants are irreversible and epilepsy is common in these infants. Inflammation may cause damage to brain cells by increasing oxygen consumption, intracellular calcium, and acidosis. In an infant with intraventricular hemorrhage (IVH), the increase of HIF-1a and HVCN1can reduce the complication of oxygen consumption and acidosis as well as by decrease of S100B can protect nerve cells from apoptosis and epilepsy through less brain damage. In this study, we investigated apoptosis in hypoxic mice influenced by miR-138-siRNAs-HIF-1a and miR-21-siRNAs-HVCN1. Methods YKL40, HIF-1a, HVCN1, and S100b genes were compared between two groups of preterm infants with and without maternal inflammation on the firth and the third day of birth, and also they were followup up three months later to observe their seizures. Then, we transfected miRNAs into cell lines to detect the changes in YKL40, HIF-1a, HVCN1, and S100b genes expression and nerve cell apoptosis. By using specific siRNAs injected in mice, we increased the expression of HIF-1a and HVCN1 and decreased S100b genes. Changes in gene expression were assessed using real-time PCR, Western blotting, flow cytometry (FCM), and immunohistochemistry (IHC). Results The expression of the HVCN1 gene revealed a strong negative correlation with epilepsy in both groups of newborns (P < 0.001). The expression levels of the S100b, YKL40, and HIF-1a genes were significantly correlated with epilepsy (P < 0.001). By FCM, the apoptotic index (A.I.) was 41.6 ± 3.3 and 34.5 ± 5.2% after transfecting miRNA-431 and miRNA-34a in cell lines, respectively, while the A.I. was 9.6 ± 2.7 and 7.1 ± 4.2% after transfecting miRNA-21 and miRNA-138. By using IHC double-labeling, it was determined that when hypoxic mice received simultaneous injections of miR-138-siRNAs-HIF-1a and miR-21-siRNAs-HVCN1, there was less apoptosis and epilepsy than in the hypoxia group. Conclusions By injecting miR-138-siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 simultaneously into hypoxia mice, we boosted HVCN1 and HIF-1a and decreased S100b, which reduced apoptosis and epilepsy in hypoxic mice.
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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) | 0.003 | 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".