ArticleAdvanced biomedical research2025
Serum Reproductive Hormone Profiles and Endometrial Expression of miR-16-5p,
Article in Advanced biomedical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Background: AngiomiRs, a group of microRNAs, target angiogenesis-related genes such as Materials and Methods: Forty adult female mice were divided into four groups: control (no intervention), progesterone (1 mg/mouse of progesterone intraperitoneally [IP] for 3 consecutive days, 72 h after day 0), EGCG (5 mg/kg of EGCG at 0, 24, 48, and 72 h), and progesterone + EGCG groups. Enzyme-linked immunosorbent assay (ELISA) was employed for measuring the concentration of estrogen and progesterone. Gene expression analysis of miR-16-5p and VEGF was conducted using real-time polymerase chain reaction (PCR). VEGF protein levels were assessed through immunohistochemistry (IHC) and western blot analysis, and endometrial CD31-positive cell density was evaluated by IHC. Results: The highest and lowest miR-16-5p expression and progesterone concentration were observed in the progesterone and EGCG groups, respectively. Endothelial cell density and VEGF protein increased in the progesterone group. Although EGCG treatment decreased VEGF protein CD31-positive cells, and progesterone levels. Estradiol levels notably declined in all treated groups. Changes in VEGF gene expression were not statistically significant. Conclusions: Exogenous progesterone or EGCG may influence endothelial cell proliferation by altering steroid hormone concentrations, miR-16-5p synthesis, and the post-transcriptional regulation of VEGF expression. However, further studies are required, particularly to explore other angiogenesis-related factors.
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