ArticleOxidative medicine and cellular longevity2019
MicroRNA-33-3p Regulates Vein Endothelial Cell Apoptosis in Selenium-Deficient Broilers by Targeting E4F1.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- miRNAs as Biomolecular Markers for Food Safety, Quality, and Traceability in Poultry Meat-A Preliminary Study.Molecules (Basel, Switzerland) · 2024Article
- Effect of selenium-enriched yeast diet on performance, biochemistry, and selenium concentration in meat and egg contents of laying Japanese quails.Archives animal breeding · 2024Article
- Co-supplementation of Vitamin K2 and Selenium Synergistically Improves Metabolic Status and Reduces Cardiovascular Risk Markers in Dyslipidemic Rabbits.Biological trace element research · 2023Article
- Transcription factor E4F1 as a regulator of cell life and disease progression.Science advances · 2023Review
- Lnc90386 Sponges miR-33-5p to MediateFrontiers in immunology · 2022Article
- Application of Selenium Conjugated to Animal Protein in Laying Hens' Diet for the Production of Selenium-Enriched Eggs.Foods (Basel, Switzerland) · 2021Article
- Review
- Effects of Dietary Selenium Sources on Physiological Status of Laying Hens and Production of Selenium-Enriched Eggs.Frontiers in nutrition · 2021Article
- MicroRNAs as Biomarkers for Animal Health and Welfare in Livestock.Frontiers in veterinary science · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenium (Se) is a type of nutrient element. The tissues of organisms can have pathological damage, including apoptosis, due to Se deficiency. Apoptosis is an important cell process and plays a key role in vascular disease and Se-deficient symptoms. In this study, the Se-deficient broiler model was duplicated, miR-33-3p in the vein was overexpressed in response to Se-deficiency, and miR-33-3p target gene E4F transcription factor 1 (E4F1) expression was also confirmed. We utilized ectopic miR-33-3p expression to validate its function for apoptosis. The results showed that miR-33-3p-targeted E4F1 are involved in the glucose-regulated protein 78- (GRP78-) induced endoplasmic reticulum stress (ERS) apoptosis pathway. We presumed that Se deficiency might trigger apoptosis via downregulating miR-33-3p. Interestingly, the miR-33-3p inhibitor and VER-155008 (GRP78 inhibitor) partly hindered the apoptosis caused by Se deficiency. Thus, the above information provides a new avenue toward understanding the mechanism of Se deficiency and reveals a novel apoptotic injury regulation model in vascular disease.
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