Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism
Background/Aims: Obesity and the related metabolic syndrome have emerged as major public health issues in modern society. miRNAs have been shown to play key roles in regulating obesity-related metabolic syndrome, and some miRNAs regulated by adiponectin were identified as novel targets for controlli...
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Format: | Article |
Language: | English |
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Cell Physiol Biochem Press GmbH & Co KG
2014-05-01
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Series: | Cellular Physiology and Biochemistry |
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Online Access: | http://www.karger.com/Article/FullText/362957 |
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author | Xinye Jiang Mei Xue Ziyi Fu Chenbo Ji Xirong Guo Lu Zhu Lulian Xu Lingxia Pang Meiyu Xu Hongming Qu |
author_facet | Xinye Jiang Mei Xue Ziyi Fu Chenbo Ji Xirong Guo Lu Zhu Lulian Xu Lingxia Pang Meiyu Xu Hongming Qu |
author_sort | Xinye Jiang |
collection | DOAJ |
description | Background/Aims: Obesity and the related metabolic syndrome have emerged as major public health issues in modern society. miRNAs have been shown to play key roles in regulating obesity-related metabolic syndrome, and some miRNAs regulated by adiponectin were identified as novel targets for controlling adipose tissue inflammation. miR-378 is a candidate target that was shown to be involved in adipose differentiation, mitochondrial metabolism and systemic energy homeostasis. However, little is known about the regulatory mechanisms of miR-378 expression. To better understand the physiological role of miR-378 in obesity and metabolic syndrome, it is crucial that we understand the regulation of miR-378 gene expression in human adipocytes. Methods: In this study, we investigated the effects of adipokines and inflammatory cytokines on miR-378 expression using Real-time PCR and the potential regulatory mechanisms using luciferase reporter assays and electrophoretic mobility shift assay (EMSA). Results: We found that adipokines and cytokines upregulated miR-378 expression primarily through SREBP and C/EBP binding sites in the miR-378 promoter region. Conclusion: Our findings showed that adipokines induced miR-378 expression and revealed the most likely mechanism of adipokine-induced miR-378 dysregulation in human adipocytes. miRNAs have been shown to function in regulating obesity-related metabolic syndrome, and miR-378 may be a novel target for controlling adipose tissue inflammation. This study offers a theoretical basis for understanding systemic adipose tissue inflammation and may provide new strategies for clinical treatment. |
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institution | Directory Open Access Journal |
issn | 1015-8987 1421-9778 |
language | English |
last_indexed | 2024-12-22T04:49:10Z |
publishDate | 2014-05-01 |
publisher | Cell Physiol Biochem Press GmbH & Co KG |
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series | Cellular Physiology and Biochemistry |
spelling | doaj.art-83c3da88a14c4fa3a8cd7ba7d43644f22022-12-21T18:38:31ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782014-05-013361778178810.1159/000362957362957Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying MechanismXinye JiangMei XueZiyi FuChenbo JiXirong GuoLu ZhuLulian XuLingxia PangMeiyu XuHongming QuBackground/Aims: Obesity and the related metabolic syndrome have emerged as major public health issues in modern society. miRNAs have been shown to play key roles in regulating obesity-related metabolic syndrome, and some miRNAs regulated by adiponectin were identified as novel targets for controlling adipose tissue inflammation. miR-378 is a candidate target that was shown to be involved in adipose differentiation, mitochondrial metabolism and systemic energy homeostasis. However, little is known about the regulatory mechanisms of miR-378 expression. To better understand the physiological role of miR-378 in obesity and metabolic syndrome, it is crucial that we understand the regulation of miR-378 gene expression in human adipocytes. Methods: In this study, we investigated the effects of adipokines and inflammatory cytokines on miR-378 expression using Real-time PCR and the potential regulatory mechanisms using luciferase reporter assays and electrophoretic mobility shift assay (EMSA). Results: We found that adipokines and cytokines upregulated miR-378 expression primarily through SREBP and C/EBP binding sites in the miR-378 promoter region. Conclusion: Our findings showed that adipokines induced miR-378 expression and revealed the most likely mechanism of adipokine-induced miR-378 dysregulation in human adipocytes. miRNAs have been shown to function in regulating obesity-related metabolic syndrome, and miR-378 may be a novel target for controlling adipose tissue inflammation. This study offers a theoretical basis for understanding systemic adipose tissue inflammation and may provide new strategies for clinical treatment.http://www.karger.com/Article/FullText/362957AdiposeInflammation factormicroRNAMechanism |
spellingShingle | Xinye Jiang Mei Xue Ziyi Fu Chenbo Ji Xirong Guo Lu Zhu Lulian Xu Lingxia Pang Meiyu Xu Hongming Qu Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism Cellular Physiology and Biochemistry Adipose Inflammation factor microRNA Mechanism |
title | Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism |
title_full | Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism |
title_fullStr | Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism |
title_full_unstemmed | Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism |
title_short | Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism |
title_sort | insight into the effects of adipose tissue inflammation factors on mir 378 expression and the underlying mechanism |
topic | Adipose Inflammation factor microRNA Mechanism |
url | http://www.karger.com/Article/FullText/362957 |
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