The Experts below are selected from a list of 276 Experts worldwide ranked by ideXlab platform
Xiaolin Niu - One of the best experts on this subject based on the ideXlab platform.
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Integrated analysis of microRNA and mRNA expression profiles in rats with Selenium Deficiency and identification of associated miRNA-mRNA network.
Scientific reports, 2018Co-Authors: Yanjing Feng, Yunjie Xing, Zhongwei Liu, Guang Yang, Xiaolin Niu, Dengfeng GaoAbstract:Selenium Deficiency is closely related with various type of cardiovascular disease. However, the miRNA-mRNA regulatory network in Selenium Deficiency related cardiac change remains to be understand. In the present study, a reliable Selenium Deficiency rat model was established and confirmed by pathological and biochemical examination. The mRNA and miRNA expression profiles were conducted by microarray technology. Gene Ontology (GO) Analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway Analysis was performed to investigate the function of targeted genes, and the relationship between miRNA and mRNA was studied by network analysis. A total of 4931 mRNAs and 119 miRNAs was differentially expressed between any two groups (control group, low-Selenium group and Selenium supplementation group). GO and KEGG pathway analysis of selected miRNAs target genes found that Selenium Deficiency was related to several different biological processes. Furthermore, a miRNA-mRNA regulatory network was conducted to illustrate the interaction of miRNAs and these targeted genes. In conclusion, our present study provides a new insight that potential molecular mechanism of Selenium Deficiency was a multiply miRNAs and mRNA caused biological change.
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microrna expression profiles in rats with Selenium Deficiency and the possible role of the wnt β catenin signaling pathway in cardiac dysfunction
International Journal of Molecular Medicine, 2015Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
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MicroRNA expression profiles in rats with Selenium Deficiency and the possible role of the Wnt/β-catenin signaling pathway in cardiac dysfunction.
International journal of molecular medicine, 2014Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
James S. M. Cuffe - One of the best experts on this subject based on the ideXlab platform.
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Maternal Selenium Deficiency in Mice Alters Offspring Glucose Metabolism and Thyroid Status in a Sexually Dimorphic Manner
Nutrients, 2020Co-Authors: Pierre Hofstee, Daniel R. Mckeating, Lucy A. Bartho, Stephen T. Anderson, Anthony V. Perkins, James S. M. CuffeAbstract:Selenium is an essential micronutrient commonly deficient in human populations. Selenium Deficiency increases the risks of pregnancy complications; however, the long-term impact of Selenium Deficiency on offspring disease remains unclear. This study investigates the effects of Selenium Deficiency during pregnancy on offspring metabolic function. Female C57BL/6 mice were allocated to control (>190 μg Selenium/kg, n = 8) or low Selenium (
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maternal Selenium Deficiency in mice alters offspring glucose metabolism and thyroid status in a sexually dimorphic manner
Nutrients, 2020Co-Authors: Pierre Hofstee, Daniel R. Mckeating, Lucy A. Bartho, Stephen T. Anderson, Anthony V. Perkins, James S. M. CuffeAbstract:Selenium is an essential micronutrient commonly deficient in human populations. Selenium Deficiency increases the risks of pregnancy complications; however, the long-term impact of Selenium Deficiency on offspring disease remains unclear. This study investigates the effects of Selenium Deficiency during pregnancy on offspring metabolic function. Female C57BL/6 mice were allocated to control (>190 μg Selenium/kg, n = 8) or low Selenium (<50 μg Selenium/kg, n = 8) diets prior to mating and throughout gestation. At postnatal day (PN) 170, mice underwent an intraperitoneal glucose tolerance test and were culled at PN180 for biochemical analysis. Mice exposed to Selenium Deficiency in utero had reduced fasting blood glucose but increased postprandial blood glucose concentrations. Male offspring from Selenium-deficient litters had increased plasma insulin levels in conjunction with reduced plasma thyroxine (tetraiodothyronine or T4) concentrations. Conversely, females exposed to Selenium Deficiency in utero exhibited increased plasma thyroxine levels with no change in plasma insulin. This study demonstrates the importance of adequate Selenium intake around pregnancy for offspring metabolic health. Given the increasing prevalence of metabolic disease, this study highlights the need for appropriate micronutrient intake during pregnancy to ensure a healthy start to life.
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maternal Selenium Deficiency during pregnancy in mice increases thyroid hormone concentrations alters placental function and reduces fetal growth
The Journal of Physiology, 2019Co-Authors: Pierre Hofstee, Daniel R. Mckeating, Lucy A. Bartho, Anthony V. Perkins, Filip Radenkovic, Georgia Mcenroe, Joshua J Fisher, Olivia J Holland, Jessica J Vanderlelie, James S. M. CuffeAbstract:Key points : Inappropriate intake of key micronutrients in pregnancy is known to alter maternal endocrine status, impair placental development and induce fetal growth restriction. Selenium is an essential micronutrient required for the function of approximately 25 important proteins. However, the specific effects of Selenium Deficiency during pregnancy on maternal, placental and fetal outcomes are poorly understood. The present study demonstrates that maternal Selenium Deficiency increases maternal triiodothyronine and tetraiodothyronine concentrations, reduces fetal blood glucose concentrations, and induces fetal growth restriction. Placental expression of key Selenium-dependent thyroid hormone converting enzymes were reduced, whereas the expression of key placental nutrient transporters was dysregulated. Selenium Deficiency had minimal impact on Selenium-dependent anti-oxidants but increased placental copper concentrations and expression of superoxide dismutase 1. These results highlight the idea that Selenium Deficiency during pregnancy may contribute to thyroid dysfunction, causing reduced fetal growth, that may precede programmed disease outcomes in offspring. Abstract : Selenium is a trace element fundamental to diverse homeostatic processes, including anti-oxidant regulation and thyroid hormone metabolism. Selenium Deficiency in pregnancy is common and increases the risk of pregnancy complications including fetal growth restriction. Although altered placental formation may contribute to these poor outcomes, the mechanism by which Selenium Deficiency contributes to complications in pregnancy is poorly understood. Female C57BL/6 mice were randomly allocated to control (>190 µg kg–1, n = 8) or low Selenium (<50 µg kg–1, n = 8) diets 4 weeks prior to mating and throughout gestation. Pregnant mice were killed at embryonic day 18.5 followed by collection of maternal and fetal tissue. Maternal and fetal plasma thyroid hormone concentrations were analysed, as was placental expression of key selenoproteins involved in thyroid metabolism and anti-oxidant defences. Selenium Deficiency increased plasma tetraiodothyronine and triiodothyronine concentrations. This was associated with a reduction in placental expression of key selenodependent deiodinases, DIO2 and DIO3. Placental expression of Selenium-dependent anti-oxidants was unaffected by Selenium Deficiency. Selenium Deficiency reduced fetal glucose concentrations, leading to reduced fetal weight. Placental glycogen content was increased within the placenta, as was Slc2a3 mRNA expression. This is the first study to demonstrate that Selenium Deficiency may reduce fetal weight through increased maternal thyroid hormone concentrations, impaired placental thyroid hormone metabolism and dysregulated placental nutrient transporter expression. The study suggests that the magnitude of Selenium Deficiency commonly reported in pregnant women may be sufficient to impair thyroid metabolism but not placental anti-oxidant concentrations.
Yujie Xing - One of the best experts on this subject based on the ideXlab platform.
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microrna expression profiles in rats with Selenium Deficiency and the possible role of the wnt β catenin signaling pathway in cardiac dysfunction
International Journal of Molecular Medicine, 2015Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
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MicroRNA expression profiles in rats with Selenium Deficiency and the possible role of the Wnt/β-catenin signaling pathway in cardiac dysfunction.
International journal of molecular medicine, 2014Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
Dengfeng Gao - One of the best experts on this subject based on the ideXlab platform.
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Integrated analysis of microRNA and mRNA expression profiles in rats with Selenium Deficiency and identification of associated miRNA-mRNA network.
Scientific reports, 2018Co-Authors: Yanjing Feng, Yunjie Xing, Zhongwei Liu, Guang Yang, Xiaolin Niu, Dengfeng GaoAbstract:Selenium Deficiency is closely related with various type of cardiovascular disease. However, the miRNA-mRNA regulatory network in Selenium Deficiency related cardiac change remains to be understand. In the present study, a reliable Selenium Deficiency rat model was established and confirmed by pathological and biochemical examination. The mRNA and miRNA expression profiles were conducted by microarray technology. Gene Ontology (GO) Analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway Analysis was performed to investigate the function of targeted genes, and the relationship between miRNA and mRNA was studied by network analysis. A total of 4931 mRNAs and 119 miRNAs was differentially expressed between any two groups (control group, low-Selenium group and Selenium supplementation group). GO and KEGG pathway analysis of selected miRNAs target genes found that Selenium Deficiency was related to several different biological processes. Furthermore, a miRNA-mRNA regulatory network was conducted to illustrate the interaction of miRNAs and these targeted genes. In conclusion, our present study provides a new insight that potential molecular mechanism of Selenium Deficiency was a multiply miRNAs and mRNA caused biological change.
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microrna expression profiles in rats with Selenium Deficiency and the possible role of the wnt β catenin signaling pathway in cardiac dysfunction
International Journal of Molecular Medicine, 2015Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
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MicroRNA expression profiles in rats with Selenium Deficiency and the possible role of the Wnt/β-catenin signaling pathway in cardiac dysfunction.
International journal of molecular medicine, 2014Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
Guang Yang - One of the best experts on this subject based on the ideXlab platform.
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Integrated analysis of microRNA and mRNA expression profiles in rats with Selenium Deficiency and identification of associated miRNA-mRNA network.
Scientific reports, 2018Co-Authors: Yanjing Feng, Yunjie Xing, Zhongwei Liu, Guang Yang, Xiaolin Niu, Dengfeng GaoAbstract:Selenium Deficiency is closely related with various type of cardiovascular disease. However, the miRNA-mRNA regulatory network in Selenium Deficiency related cardiac change remains to be understand. In the present study, a reliable Selenium Deficiency rat model was established and confirmed by pathological and biochemical examination. The mRNA and miRNA expression profiles were conducted by microarray technology. Gene Ontology (GO) Analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway Analysis was performed to investigate the function of targeted genes, and the relationship between miRNA and mRNA was studied by network analysis. A total of 4931 mRNAs and 119 miRNAs was differentially expressed between any two groups (control group, low-Selenium group and Selenium supplementation group). GO and KEGG pathway analysis of selected miRNAs target genes found that Selenium Deficiency was related to several different biological processes. Furthermore, a miRNA-mRNA regulatory network was conducted to illustrate the interaction of miRNAs and these targeted genes. In conclusion, our present study provides a new insight that potential molecular mechanism of Selenium Deficiency was a multiply miRNAs and mRNA caused biological change.
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microrna expression profiles in rats with Selenium Deficiency and the possible role of the wnt β catenin signaling pathway in cardiac dysfunction
International Journal of Molecular Medicine, 2015Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.
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MicroRNA expression profiles in rats with Selenium Deficiency and the possible role of the Wnt/β-catenin signaling pathway in cardiac dysfunction.
International journal of molecular medicine, 2014Co-Authors: Yujie Xing, Zhongwei Liu, Guang Yang, Dengfeng Gao, Xiaolin NiuAbstract:Selenium Deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during Selenium Deficiency and whether Selenium Deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, Selenium-deficient rats and Selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with Selenium Deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with Selenium Deficiency. In conclusion, the possible mechanism of Selenium Deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.