MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11

ABSTRACT: Selenium (Se) has been proven to be an essential trace element for organism. Se deficiency in poultry can cause widespread damage, such as exudative diathesis. The liver is not only the main organ of metabolism, but also one of the organs with high Se content in organism. Recent studies ha...

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Main Authors: Kaixin Zhang, Xuedie Gu, Yu Xia, Xiaochun Zhao, Ahmed Khoso Pervez, Shu Li
Format: Article
Language:English
Published: Elsevier 2023-01-01
Series:Poultry Science
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0032579122005661
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author Kaixin Zhang
Xuedie Gu
Yu Xia
Xiaochun Zhao
Ahmed Khoso Pervez
Shu Li
author_facet Kaixin Zhang
Xuedie Gu
Yu Xia
Xiaochun Zhao
Ahmed Khoso Pervez
Shu Li
author_sort Kaixin Zhang
collection DOAJ
description ABSTRACT: Selenium (Se) has been proven to be an essential trace element for organism. Se deficiency in poultry can cause widespread damage, such as exudative diathesis. The liver is not only the main organ of metabolism, but also one of the organs with high Se content in organism. Recent studies have shown that solute carrier family 7 member 11 (SLC7A11) plays a key role in the negative regulation of ferroptosis. In order to explore the mechanism of Se deficiency induces liver ferroptosis in broilers, and the role of microRNAs (miRNAs) in this process, we divided broilers into 2 groups: control group (0.2 mg/kg Se) and Se deficiency group (0.03 mg/kg Se). Hematoxylin-Eosin staining detected liver tissue damage in broilers. Predicted and verified the targeting relationship between miR-129-3p and SLC7A11 through miRDB and dual luciferase report experiments. The genes related to ferroptosis were detected by qRT-PCR and Western Blot. The results showed that the expression level of miR-129-3p mRNA in Se-deficient liver was significantly increased. To understand whether the miR-129-3p/SLC7A11 axis could involve in the process of ferroptosis, our further research showed that overexpression of miR-129-3p could reduce the expression of SLC7A11 and its downstream GCL, GSS, and GPX4, thereby inducing ferroptosis. These data indicates that miR-129-3p affected ferroptosis under Se deficiency conditions through the SLC7A11 pathway. Our research provides a new perspective for the mechanism of Se deficiency on the liver damage.
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spelling doaj.art-b659de04d6854ef08d9515f3adc490212022-12-22T03:43:38ZengElsevierPoultry Science0032-57912023-01-011021102271MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11Kaixin Zhang0Xuedie Gu1Yu Xia2Xiaochun Zhao3Ahmed Khoso Pervez4Shu Li5College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. ChinaAnimal Disease Control and Prevention of Heilongjiang Province, Harbin 150069, ChinaShaheed Benazir Bhutto, University of Veterinary and Animal Sciences, Sakrand, PakistanCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China; Corresponding author:ABSTRACT: Selenium (Se) has been proven to be an essential trace element for organism. Se deficiency in poultry can cause widespread damage, such as exudative diathesis. The liver is not only the main organ of metabolism, but also one of the organs with high Se content in organism. Recent studies have shown that solute carrier family 7 member 11 (SLC7A11) plays a key role in the negative regulation of ferroptosis. In order to explore the mechanism of Se deficiency induces liver ferroptosis in broilers, and the role of microRNAs (miRNAs) in this process, we divided broilers into 2 groups: control group (0.2 mg/kg Se) and Se deficiency group (0.03 mg/kg Se). Hematoxylin-Eosin staining detected liver tissue damage in broilers. Predicted and verified the targeting relationship between miR-129-3p and SLC7A11 through miRDB and dual luciferase report experiments. The genes related to ferroptosis were detected by qRT-PCR and Western Blot. The results showed that the expression level of miR-129-3p mRNA in Se-deficient liver was significantly increased. To understand whether the miR-129-3p/SLC7A11 axis could involve in the process of ferroptosis, our further research showed that overexpression of miR-129-3p could reduce the expression of SLC7A11 and its downstream GCL, GSS, and GPX4, thereby inducing ferroptosis. These data indicates that miR-129-3p affected ferroptosis under Se deficiency conditions through the SLC7A11 pathway. Our research provides a new perspective for the mechanism of Se deficiency on the liver damage.http://www.sciencedirect.com/science/article/pii/S0032579122005661selenium deficiencyferroptosismiR-129-3pSLC7A11broiler liver
spellingShingle Kaixin Zhang
Xuedie Gu
Yu Xia
Xiaochun Zhao
Ahmed Khoso Pervez
Shu Li
MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
Poultry Science
selenium deficiency
ferroptosis
miR-129-3p
SLC7A11
broiler liver
title MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
title_full MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
title_fullStr MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
title_full_unstemmed MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
title_short MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11
title_sort mir 129 3p regulates ferroptosis in the liver of selenium deficient broilers by targeting slc7a11
topic selenium deficiency
ferroptosis
miR-129-3p
SLC7A11
broiler liver
url http://www.sciencedirect.com/science/article/pii/S0032579122005661
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AT yuxia mir1293pregulatesferroptosisintheliverofseleniumdeficientbroilersbytargetingslc7a11
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