The Experts below are selected from a list of 19896 Experts worldwide ranked by ideXlab platform
Philip S Tsao - One of the best experts on this subject based on the ideXlab platform.
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abstract 19986 microRNA 29b is a regulator and therapeutic target of aortic stiffness in type 2 diabetes
Circulation, 2016Co-Authors: Isabel N Schellinger, Lars Maegdefessel, Philip S Tsao, Joshua M Spin, Karin Mattern, Lena Mattes, Gerd Hasenfus, Uwe RaazAbstract:Introduction: Accelerated arterial stiffening is a common complication of type 2 diabetes that is patho-mechanistically linked to a severely increased cardiovascular risk. Unfortunately, up to date...
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microRNA 29b regulation of abdominal aortic aneurysm development
Trends in Cardiovascular Medicine, 2014Co-Authors: Lars Maegdefessel, Junya Azuma, Philip S TsaoAbstract:Tremendous efforts have been initiated to elucidate the molecular and pathophysiological characteristics of abdominal aortic aneurysm (AAA) disease, which is a significant contributor to morbidity and mortality in the Western world. Recently, a novel class of small noncoding RNAs, called microRNAs, was identified as important transcriptional and posttranscriptional inhibitors of gene expression thought to simultaneously "fine tune" the translational output of multiple target messenger RNAs (mRNAs) by promoting mRNA degradation or inhibiting translation. Several research groups were able to identify the miR-29 family, and miR-29b in particular, as crucial regulators of-not only vascular fibrosis-but also cardiac-, kidney-, liver-, and skin-fibrosis. The current review briefly points out data indicating a causal role for miR-29 in various diseases, while focusing on its potential benefit during AAA initiation and propagation.
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abstract 82 tgf β regulates matrix production in aortic fibroblasts through microRNA 29b
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Joshua M Spin, Lars Maegdefessel, Junya Azuma, Ryuji Toh, Alicia Deng, Philip S TsaoAbstract:Abdominal aortic aneurysms (AAA) cause ∼15,000 annual deaths in the United States. The mechanisms of AAA expansion remain incompletely explored. microRNAs (miRs) regulate gene expression post-transcriptionally, and play crucial roles in vascular integrity. TGF-β can act as a profibrotic stimulus, is a known regulator of miR-29b expression in some cell types, and may play a protective role in AAA development. Numerous extracellular matrix genes are predicted targets of miR-29b. We have previously shown that miR-29b is decreased in both human AAA, and in aneurysmal aortic segments in murine AAA models. Further inhibition of miR-29b in vivo reduces abdominal aortic aneurysm progression in two murine AAA models: the porcine-pancreatic-elastase (PPE) model in C57Bl/6 mice, and the angiotensin II-infusion (AngII) model in ApoE -/- mice, and is associated with a pro-fibrotic response within the vessel wall. We performed vascular cell culture studies using human aortic adventitial fibroblasts (AAFs) and aortic smooth muscle cells (ASMCs) to evaluate the expression and regulation of miR-29b. Treatment with recombinant human TGFβ1 significantly decreased miR-29b levels in aortic adventitial fibroblasts, but not smooth muscle cells (vs. untreated cells). TGFβ1 treatment increased soluble collagen production by AAFs nearly 4-fold, and increased gene expression of COL1A1 and COL3A1 . In ASMCs, TGFβ1 primarily increased ELN expression, and COL1A1 and COL3A1 to a lesser extent. We altered miR-29b expression in vitro by transfecting AAFs and ASMCs with either an antagomir (anti-29b) to inhibit activity or a pre-miR (pre-29b) to enhance activity (vs. scrambled miR control). Successful transfection (>50% of all cells) was confirmed by visual fluorescent microscopic analysis and FACS for labeled tag. Anti-29b significantly augmented the effects of TGFβ treatment upon soluble collagen protein levels and collagen gene expression in AAFs, while pre-29b inhibited this response nearly to untreated-control levels. A similar gene expression response was seen in ASMCs. These data suggest that TGFβ regulation of miR-29b in aortic fibroblasts leads to a profibrotic response, partly explaining its protective effects in AAA development.
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abstract 16283 nicotine augmented abdominal aortic aneurysms are regulated by microRNA 29b
Circulation, 2011Co-Authors: Lars Maegdefessel, Junya Azuma, Denis R Merk, Alicia Deng, Ryuji M Toh, Jocelyn P Chin, Joshua M Spin, Philip S TsaoAbstract:More than 90% of patients with an abdominal aortic aneurysm (AAA) report a history of smoking. microRNAs (miRs) regulate gene expression on the post-transcriptional level and play crucial roles in ...
Lin Tian - One of the best experts on this subject based on the ideXlab platform.
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model
Elsevier, 2019Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis. Keywords: microRNA-29b, mesenchymal-epithelial transition, silicosis, epithelial-mesenchymal transition, lung functio
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
Molecular therapy. Nucleic acids, 2018Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.
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microRNA 29b inhibits supernatants from silica treated macrophages from inducing extracellular matrix synthesis in lung fibroblasts
Toxicology Research, 2017Co-Authors: Ximeng Lian, Jingping Sun, Zhonghui Zhu, Xiaowei Chen, Yan Wang, Piye Niu, Lin TianAbstract:Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM) components. The ECM is mainly secreted by myofibroblasts which are the activated state of fibroblasts. microRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified. In this study, we hypothesized that miR-29b might play a protective role in the progression of silicosis. MTT assay, qRT-PCR, immunofluorescence and western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Meanwhile they could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited ECM synthesis. These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.
Yan Wang - One of the best experts on this subject based on the ideXlab platform.
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microRNA 29b 3p targets sparc gene to protect cardiocytes against autophagy and apoptosis in hypoxic induced h9c2 cells
Journal of Cardiovascular Translational Research, 2019Co-Authors: Shu Zhou, Dazhou Lei, Hongqiang Han, Shucai Zhao, Yan WangAbstract:microRNAs participate in the regulation of abnormal cardiomyocyte apoptosis and autophagy, which leads to heart failure (HF). Lower miR-29b-3p levels were found in HF patients in this study. However, the role of miR-29b-3p in the molecular pathogenesis of HF remains unclear. Hypoxia-stimulated H9c2 cells were used an in vitro model of HF. It was found that hypoxia stimulation decreased the miR-29b-3p expression and enhanced cell apoptosis and autophagy response in H9c2 cells. While the effects of hypoxia on cell apoptosis and autophagy were reversed by miR-29b-3p transfection, especially 100 nM. The secreted protein acidic and rich in cysteine (SPARC), predicted as a direct target of miR-29b-3p, aggravated the hypoxia-induced cells apoptosis, autophagy, and TGFβ1/Smad3 activation. While the changes were dramatically reversed by miR-29b-3p. Taken together, our data suggest that miR-29b-3p plays an important role in the progression of HF through targeting SPARC and regulating TGFβ1/Smad3 pathway.
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effect of microRNA 29b on proliferation migration and invasion of endometrial cancer cells
Journal of International Medical Research, 2019Co-Authors: Jian Kong, Yan WangAbstract:ObjectiveAberrant expression of microRNAs is a key regulator of tumorigenesis and progression in endometrial cancer. We assessed the effect of microRNA-29b (miR-29b) on proliferation, chemosensitiv...
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model
Elsevier, 2019Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis. Keywords: microRNA-29b, mesenchymal-epithelial transition, silicosis, epithelial-mesenchymal transition, lung functio
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
Molecular therapy. Nucleic acids, 2018Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.
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microRNA 29b inhibits supernatants from silica treated macrophages from inducing extracellular matrix synthesis in lung fibroblasts
Toxicology Research, 2017Co-Authors: Ximeng Lian, Jingping Sun, Zhonghui Zhu, Xiaowei Chen, Yan Wang, Piye Niu, Lin TianAbstract:Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM) components. The ECM is mainly secreted by myofibroblasts which are the activated state of fibroblasts. microRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified. In this study, we hypothesized that miR-29b might play a protective role in the progression of silicosis. MTT assay, qRT-PCR, immunofluorescence and western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Meanwhile they could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited ECM synthesis. These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.
Lars Maegdefessel - One of the best experts on this subject based on the ideXlab platform.
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abstract 19986 microRNA 29b is a regulator and therapeutic target of aortic stiffness in type 2 diabetes
Circulation, 2016Co-Authors: Isabel N Schellinger, Lars Maegdefessel, Philip S Tsao, Joshua M Spin, Karin Mattern, Lena Mattes, Gerd Hasenfus, Uwe RaazAbstract:Introduction: Accelerated arterial stiffening is a common complication of type 2 diabetes that is patho-mechanistically linked to a severely increased cardiovascular risk. Unfortunately, up to date...
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microRNA 29b regulation of abdominal aortic aneurysm development
Trends in Cardiovascular Medicine, 2014Co-Authors: Lars Maegdefessel, Junya Azuma, Philip S TsaoAbstract:Tremendous efforts have been initiated to elucidate the molecular and pathophysiological characteristics of abdominal aortic aneurysm (AAA) disease, which is a significant contributor to morbidity and mortality in the Western world. Recently, a novel class of small noncoding RNAs, called microRNAs, was identified as important transcriptional and posttranscriptional inhibitors of gene expression thought to simultaneously "fine tune" the translational output of multiple target messenger RNAs (mRNAs) by promoting mRNA degradation or inhibiting translation. Several research groups were able to identify the miR-29 family, and miR-29b in particular, as crucial regulators of-not only vascular fibrosis-but also cardiac-, kidney-, liver-, and skin-fibrosis. The current review briefly points out data indicating a causal role for miR-29 in various diseases, while focusing on its potential benefit during AAA initiation and propagation.
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abstract 82 tgf β regulates matrix production in aortic fibroblasts through microRNA 29b
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Joshua M Spin, Lars Maegdefessel, Junya Azuma, Ryuji Toh, Alicia Deng, Philip S TsaoAbstract:Abdominal aortic aneurysms (AAA) cause ∼15,000 annual deaths in the United States. The mechanisms of AAA expansion remain incompletely explored. microRNAs (miRs) regulate gene expression post-transcriptionally, and play crucial roles in vascular integrity. TGF-β can act as a profibrotic stimulus, is a known regulator of miR-29b expression in some cell types, and may play a protective role in AAA development. Numerous extracellular matrix genes are predicted targets of miR-29b. We have previously shown that miR-29b is decreased in both human AAA, and in aneurysmal aortic segments in murine AAA models. Further inhibition of miR-29b in vivo reduces abdominal aortic aneurysm progression in two murine AAA models: the porcine-pancreatic-elastase (PPE) model in C57Bl/6 mice, and the angiotensin II-infusion (AngII) model in ApoE -/- mice, and is associated with a pro-fibrotic response within the vessel wall. We performed vascular cell culture studies using human aortic adventitial fibroblasts (AAFs) and aortic smooth muscle cells (ASMCs) to evaluate the expression and regulation of miR-29b. Treatment with recombinant human TGFβ1 significantly decreased miR-29b levels in aortic adventitial fibroblasts, but not smooth muscle cells (vs. untreated cells). TGFβ1 treatment increased soluble collagen production by AAFs nearly 4-fold, and increased gene expression of COL1A1 and COL3A1 . In ASMCs, TGFβ1 primarily increased ELN expression, and COL1A1 and COL3A1 to a lesser extent. We altered miR-29b expression in vitro by transfecting AAFs and ASMCs with either an antagomir (anti-29b) to inhibit activity or a pre-miR (pre-29b) to enhance activity (vs. scrambled miR control). Successful transfection (>50% of all cells) was confirmed by visual fluorescent microscopic analysis and FACS for labeled tag. Anti-29b significantly augmented the effects of TGFβ treatment upon soluble collagen protein levels and collagen gene expression in AAFs, while pre-29b inhibited this response nearly to untreated-control levels. A similar gene expression response was seen in ASMCs. These data suggest that TGFβ regulation of miR-29b in aortic fibroblasts leads to a profibrotic response, partly explaining its protective effects in AAA development.
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inhibition of microRNA 29b reduces murine abdominal aortic aneurysm development
Journal of Clinical Investigation, 2012Co-Authors: Lars Maegdefessel, Junya Azuma, Ryuji Toh, Denis R Merk, Alicia Deng, Jocelyn T Chin, Uwe Raaz, Anke M Schoelmerich, Azad Raiesdana, Nicholas J LeeperAbstract:microRNAs (miRs) regulate gene expression at the posttranscriptional level and play crucial roles in vascular integrity. As such, they may have a role in modifying abdominal aortic aneurysm (AAA) expansion, the pathophysiological mechanisms of which remain incompletely explored. Here, we investigate the role of miRs in 2 murine models of experimental AAA: the porcine pancreatic elastase (PPE) infusion model in C57BL/6 mice and the AngII infusion model in Apoe-/- mice. AAA development was accompanied by decreased aortic expression of miR-29b, along with increased expression of known miR-29b targets, Col1a1, Col3a1, Col5a1, and Eln, in both models. In vivo administration of locked nucleic acid anti-miR-29b greatly increased collagen expression, leading to an early fibrotic response in the abdominal aortic wall and resulting in a significant reduction in AAA progression over time in both models. In contrast, overexpression of miR-29b using a lentiviral vector led to augmented AAA expansion and significant increase of aortic rupture rate. Cell culture studies identified aortic fibroblasts as the likely vascular cell type mediating the profibrotic effects of miR-29b modulation. A similar pattern of reduced miR-29b expression and increased target gene expression was observed in human AAA tissue samples compared with that in organ donor controls. These data suggest that therapeutic manipulation of miR-29b and its target genes holds promise for limiting AAA disease progression and protecting from rupture.
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abstract 16283 nicotine augmented abdominal aortic aneurysms are regulated by microRNA 29b
Circulation, 2011Co-Authors: Lars Maegdefessel, Junya Azuma, Denis R Merk, Alicia Deng, Ryuji M Toh, Jocelyn P Chin, Joshua M Spin, Philip S TsaoAbstract:More than 90% of patients with an abdominal aortic aneurysm (AAA) report a history of smoking. microRNAs (miRs) regulate gene expression on the post-transcriptional level and play crucial roles in ...
Jingping Sun - One of the best experts on this subject based on the ideXlab platform.
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model
Elsevier, 2019Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis. Keywords: microRNA-29b, mesenchymal-epithelial transition, silicosis, epithelial-mesenchymal transition, lung functio
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microRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
Molecular therapy. Nucleic acids, 2018Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin TianAbstract:Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. microRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.
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microRNA 29b inhibits supernatants from silica treated macrophages from inducing extracellular matrix synthesis in lung fibroblasts
Toxicology Research, 2017Co-Authors: Ximeng Lian, Jingping Sun, Zhonghui Zhu, Xiaowei Chen, Yan Wang, Piye Niu, Lin TianAbstract:Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM) components. The ECM is mainly secreted by myofibroblasts which are the activated state of fibroblasts. microRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified. In this study, we hypothesized that miR-29b might play a protective role in the progression of silicosis. MTT assay, qRT-PCR, immunofluorescence and western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Meanwhile they could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited ECM synthesis. These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.