The Experts below are selected from a list of 657 Experts worldwide ranked by ideXlab platform
Danning Hu - One of the best experts on this subject based on the ideXlab platform.
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microRNA-182 Suppresses HGF/SF-Induced Increases in Retinal Pigment Epithelial Cell Proliferation and Migration through Targeting c-Met.
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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microRNA 182 suppresses hgf sf induced increases in retinal pigment epithelial cell proliferation and migration through targeting c met
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:: As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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role of microRNA 182 in posterior uveal melanoma regulation of tumor development through mitf bcl2 and cyclin d2
PLOS ONE, 2012Co-Authors: Xiang Da Dong, Jiao Wang, Xiaoyan Chen, Lihua Wang, Chao Wang, Danning HuAbstract:microRNAs (miRNAs) are endogenous small non-coding RNAs that play central roles in diverse pathological processes. In this study, we investigated the effect of microRNA-182 (miR-182) on the development of posterior uveal melanomas. Initially, we demonstrated that miR-182 expression was dependent on p53 induction in uveal melanoma cells. Interestingly, transient transfection of miR-182 into cultured uveal melanoma cells led to a significant decrease in cell growth, migration, and invasiveness. Cells transfected with miR-182 demonstrated cell cycle G1 arrest and increased apoptotic activity. Using bioinformatics, we identified three potential targets of miR-182, namely MITF, BCL2 and cyclin D2. miR-182 was shown to have activity on mRNA expression by targeting the 3′ untranslated region of MITF, BCL2 and cyclin D2. Subsequent Western blot analysis confirmed the downregulation of MITF, BCL2 and cyclin D2 protein expression. The expression of oncogene c-Met and its downstream Akt and ERK1/2 pathways was also downregulated by miR-182. Concordant with the findings that miR-182 was decreased in uveal melanoma tissue samples, overexpression of miR-182 also suppressed the in vivo growth of uveal melanoma cells. Our results demonstrated that miR-182, a p53 dependent miRNA, suppressed the expression of MITF, BCL2, cyclin D2 and functioned as a potent tumor suppressor in uveal melanoma cells.
Lihua Wang - One of the best experts on this subject based on the ideXlab platform.
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microRNA-182 Suppresses HGF/SF-Induced Increases in Retinal Pigment Epithelial Cell Proliferation and Migration through Targeting c-Met.
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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microRNA 182 suppresses hgf sf induced increases in retinal pigment epithelial cell proliferation and migration through targeting c met
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:: As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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role of microRNA 182 in posterior uveal melanoma regulation of tumor development through mitf bcl2 and cyclin d2
PLOS ONE, 2012Co-Authors: Xiang Da Dong, Jiao Wang, Xiaoyan Chen, Lihua Wang, Chao Wang, Danning HuAbstract:microRNAs (miRNAs) are endogenous small non-coding RNAs that play central roles in diverse pathological processes. In this study, we investigated the effect of microRNA-182 (miR-182) on the development of posterior uveal melanomas. Initially, we demonstrated that miR-182 expression was dependent on p53 induction in uveal melanoma cells. Interestingly, transient transfection of miR-182 into cultured uveal melanoma cells led to a significant decrease in cell growth, migration, and invasiveness. Cells transfected with miR-182 demonstrated cell cycle G1 arrest and increased apoptotic activity. Using bioinformatics, we identified three potential targets of miR-182, namely MITF, BCL2 and cyclin D2. miR-182 was shown to have activity on mRNA expression by targeting the 3′ untranslated region of MITF, BCL2 and cyclin D2. Subsequent Western blot analysis confirmed the downregulation of MITF, BCL2 and cyclin D2 protein expression. The expression of oncogene c-Met and its downstream Akt and ERK1/2 pathways was also downregulated by miR-182. Concordant with the findings that miR-182 was decreased in uveal melanoma tissue samples, overexpression of miR-182 also suppressed the in vivo growth of uveal melanoma cells. Our results demonstrated that miR-182, a p53 dependent miRNA, suppressed the expression of MITF, BCL2, cyclin D2 and functioned as a potent tumor suppressor in uveal melanoma cells.
Yanqing Ding - One of the best experts on this subject based on the ideXlab platform.
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microRNA 182 targets special at rich sequence binding protein 2 to promote colorectal cancer proliferation and metastasis
Journal of Translational Medicine, 2014Co-Authors: Minhui Yang, Jiang Yu, Dongmei Jiang, Wenlu Li, Shuang Wang, Yanqing DingAbstract:Background Increasing evidence has revealed that microRNAs (miRNA) played a pivotal role in regulating cancer cell proliferation and metastasis. The deregulation of miR-182 has been identified in colorectal cancer (CRC). However, the role and mechanism of miR-182 in CRC have not been completely understood yet.
Xiaoyan Chen - One of the best experts on this subject based on the ideXlab platform.
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microRNA 182 inhibits the proliferation and migration of human corneal epithelial cells
Chin J Optom Ophthalmol Vis Sci, 2018Co-Authors: Xiaoting Zhao, Xia Jing, Jiao Wang, Xiaoyan ChenAbstract:Objective: We investigated the in vivo and in vitro effects of microRNA-182 (miR-182) , which modulates post-transcriptional regulation of gene expression, on corneal epithelial cell proliferation, migration, and wound healing. Methods: In this experimental research, mouse corneal epithelial wound healing of five mouse was initiated by a scrape injury. Realtime reverse transcriptase polymerase chain reaction (RT-PCR) was performed to detect the expression level of miR-182 in the mouse corneal epithelium during the wound healing process (48 hours post scraping). Lipofectamine RNAiMAX reagent was used to transfect human corneal epithelial cells (HCECs) in vitro with either miR-182 or negative control RNA oligo. Cell proliferation assay (MTS), cell colony-forming assay, and flow cytometry were used to evaluate the effects of miR-182 on cell proliferation and cell cycle. An in vitro wound-healing assay (the HCECs were wounded by placing a scratch along the surface of each culture) was carried out to evaluate the effect of miR-182 on cell migration. Data were analyzed using independent t test. Results: The in vivo expression of miR-182 in experimentally wounded corneal epithelia was significantly lower than in the non-wounded controls (t=147.6, 79.2, 136.8, 41.3, 89.8, all P<0.001). In vitro, the relative number of cells in the experimental group transfected with miR-182 was (81±5)%, which was significantly less than that in the control group transfected with negative control RNA oligo, 100% (t=6.6, P=0.003). Further, the number of clones in the experimental group was remarkably decreased compared to that in the control group. The percentage of transfected cells in G1 arrest was (49±7)%, which was significantly higher than that in the control group, (35±4)% (t=-3.0, P=0.041). In addition, the migration distance of HCECs in the transfected cells, 99±12 μm, was shorter than in the control cells, 213±14 μm (t=10.8, P=0.001). Conclusions: miR-182 negatively regulates the corneal epithelial wound healing process by inhibiting corneal epithelial cell proliferation and migration. Key words: corneal wound healing; miR-182; corneal epithelium cell; proliferation; migration
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microRNA 182 suppresses hgf sf induced increases in retinal pigment epithelial cell proliferation and migration through targeting c met
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:: As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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microRNA-182 Suppresses HGF/SF-Induced Increases in Retinal Pigment Epithelial Cell Proliferation and Migration through Targeting c-Met.
PLOS ONE, 2016Co-Authors: Lihua Wang, Xiaoting Zhao, Xiaoyan Chen, Feng Dong, Peter S Reinach, Dandan He, Danning HuAbstract:As increases in hepatocyte growth factor/scatter factor (HGF/SF) induce retinal pigment epithelial (RPE) migration and proliferation into the vitreous cavity and contribute to proliferative vitreoretinopathy (PVR) development, we determined if changes in miR-182 expression affect such behavioral changes. We found that miR-182 expression was less in PVR clinical samples than in primary RPE cells whereas c-Met was upregulated. Ectopic miR-182 inhibited RPE cell proliferation, cell cycle, and migration. Bioinformatic analysis identified c-Met as a miR-182 target, which was confirmed with the luciferase reporter assay. Transfection of miR-182 into RPE cells induced c-Met downregulation, which led to reduced cell proliferation and migration through declines in p-Akt formation. MiR-182 downregulation along with c-Met upregulation in PVR tissues suggest that these two opposing effects play important roles in PVR development. As ectopic miR-182 expression suppressed RPE cell proliferation and migration, strategies to selectively upregulate miR-182 expression in a clinical setting may provide a novel option to treat this disease.
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role of microRNA 182 in posterior uveal melanoma regulation of tumor development through mitf bcl2 and cyclin d2
PLOS ONE, 2012Co-Authors: Xiang Da Dong, Jiao Wang, Xiaoyan Chen, Lihua Wang, Chao Wang, Danning HuAbstract:microRNAs (miRNAs) are endogenous small non-coding RNAs that play central roles in diverse pathological processes. In this study, we investigated the effect of microRNA-182 (miR-182) on the development of posterior uveal melanomas. Initially, we demonstrated that miR-182 expression was dependent on p53 induction in uveal melanoma cells. Interestingly, transient transfection of miR-182 into cultured uveal melanoma cells led to a significant decrease in cell growth, migration, and invasiveness. Cells transfected with miR-182 demonstrated cell cycle G1 arrest and increased apoptotic activity. Using bioinformatics, we identified three potential targets of miR-182, namely MITF, BCL2 and cyclin D2. miR-182 was shown to have activity on mRNA expression by targeting the 3′ untranslated region of MITF, BCL2 and cyclin D2. Subsequent Western blot analysis confirmed the downregulation of MITF, BCL2 and cyclin D2 protein expression. The expression of oncogene c-Met and its downstream Akt and ERK1/2 pathways was also downregulated by miR-182. Concordant with the findings that miR-182 was decreased in uveal melanoma tissue samples, overexpression of miR-182 also suppressed the in vivo growth of uveal melanoma cells. Our results demonstrated that miR-182, a p53 dependent miRNA, suppressed the expression of MITF, BCL2, cyclin D2 and functioned as a potent tumor suppressor in uveal melanoma cells.
Jiangtian Tian - One of the best experts on this subject based on the ideXlab platform.
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microRNA 182 promotes t helper 1 cell by repressing hypoxia induced factor 1 alpha in experimental autoimmune encephalomyelitis
European Journal of Immunology, 2019Co-Authors: Wuchun Bi, Jiangtian Tian, Shaohong Fang, Zhaoying Li, Lili Mu, Yun Zhang, Xi Wang, Yinan Qu, Jinghua Wang, Qingfei KongAbstract:: microRNA 182 is important for the clonal expansion of CD4+ T cells (Th) following IL-2 stimulation and is a potential therapeutic target for autoimmune diseases. In the present study, we investigated the role of microRNA 182 in the differentiation of pro-inflammatory CD4+ T helper cell by overexpressing or silencing microRNA 182 expression both in in vivo and in vitro settings. We report that in the studied Chinese cohort, microRNA 182 is upregulated in patients with relapse and remitting multiple sclerosis (RRMS) and this upregulation is associated with increased IFN-γ producing CD4+ Th1 cells in the circulation. In the murine experimental autoimmune encephalomyelitis (EAE) model, global microRNA 182 overexpression exacerbates clinical symptoms and results in augmented CD4+ IFN-γ+ Th1 and CD4+ IL-17+ Th17 differentiation in vivo. Addition of microRNA 182 mimics in vitro represses both the protein expression and transcriptional activity of hypoxia induced factor 1α (HIF-1α) but increases the level of IFN-γ transcripts in sorted murine CD4+ T cells. Together, our results provide evidence that microRNA 182 may be one of the transitional hubs contribution to regulate Th cells expansion in response to self-antigens and differentiation of antigen specific Th cells during the progression of autoimmune inflammations.
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microRNA 182 prevents vascular smooth muscle cell dedifferentiation via fgf9 pdgfrβ signaling
International Journal of Molecular Medicine, 2017Co-Authors: Nana Dong, Jiangtian Tian, Shaohong Fang, Wei Wang, Jinwei Tian, Bo Lv, Rui Jiang, Dan Huang, Hulun Li, Bo YuAbstract:: The abnormal phenotypic transformation of vascular smooth muscle cells (SMCs) causes various proliferative vascular diseases. microRNAs (miRNAs or miRs) have been established to play important roles in SMC biology and phenotypic modulation. This study revealed that the expression of miR‑182 was markedly altered during rat vascular SMC phenotypic transformation in vitro. We aimed to investigate the role of miR‑182 in the vascular SMC phenotypic switch and to determine the potential molecular mechanisms involved. The expression of miR‑182 gene was significantly downregulated in cultured SMCs during dedifferentiation from a contractile to a synthetic phenotype. Conversely, the upregulation of miR‑182 increased the expression of SMC-specific contractile genes, such as α-smooth muscle actin, smooth muscle 22α and calponin. Additionally, miR‑182 overexpression potently inhibited SMC proliferation and migration under both basal conditions and under platelet-derived growth factor-BB stimulation. Furthermore, we identified fibroblast growth factor 9 (FGF9) as the target gene of miR‑182 for the phenotypic modulation of SMCs mediated through platelet-derived growth factor receptor β (PDGFRβ) signaling. These data suggest that miR‑182 may be a novel SMC phenotypic marker and a modulator that may be used to prevent SMC dedifferentiation via FGF9/PDGFRβ signaling.
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microRNA-182 prevents vascular smooth muscle cell dedifferentiation via FGF9/PDGFRβ signaling
International Journal of Molecular Medicine, 2017Co-Authors: Nana Dong, Shaohong Fang, Wei Wang, Jinwei Tian, Bo Lv, Rui Jiang, Dan Huang, Jiangtian TianAbstract:The abnormal phenotypic transformation of vascular smooth muscle cells (SMCs) causes various proliferative vascular diseases. microRNAs (miRNAs or miRs) have been established to play important roles in SMC biology and phenotypic modulation. This study revealed that the expression of miR‑182 was markedly altered during rat vascular SMC phenotypic transformation in vitro. We aimed to investigate the role of miR‑182 in the vascular SMC phenotypic switch and to determine the potential molecular mechanisms involved. The expression of miR‑182 gene was significantly downregulated in cultured SMCs during dedifferentiation from a contractile to a synthetic phenotype. Conversely, the upregulation of miR‑182 increased the expression of SMC-specific contractile genes, such as α-smooth muscle actin, smooth muscle 22α and calponin. Additionally, miR‑182 overexpression potently inhibited SMC proliferation and migration under both basal conditions and under platelet-derived growth factor-BB stimulation. Furthermore, we identified fibroblast growth factor 9 (FGF9) as the target gene of miR‑182 for the phenotypic modulation of SMCs mediated through platelet-derived growth factor receptor β (PDGFRβ) signaling. These data suggest that miR‑182 may be a novel SMC phenotypic marker and a modulator that may be used to prevent SMC dedifferentiation via FGF9/PDGFRβ signaling.
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microRNA 182 inhibits cd4 cd25 foxp3 treg differentiation in experimental autoimmune encephalomyelitis
Clinical Immunology, 2016Co-Authors: Changyun Ping, Xiaoyu Shang, Jiangtian Tian, Sihan Zhao, Lei Li, Shaohong Fang, Yanfeng Zhao, Zhaoying Li, Yanwen Xu, Lili MuAbstract:microRNA 182 has been found to have a distinct contribution in the clonal expansion of activated- and functioning of specialized-helper T cells. In this study we knocked down microRNA 182 in vivo and induced experimental autoimmune encephalomyelitis (EAE) to determine the influences of microRNA 182 in the Treg cells functional specialization through Foxo1 dependent pathway in the peripheral lymphoid organs. Down-regulation of microRNA 182 significantly increased the proportions of Foxp3+ T cells in the peripheral lymph nodes and spleen. In vivo study verified a positive correlation between microRNA 182 levels and symptom severity of EAE, and a negative correlation between microRNA 182 and the transcriptional factor Foxp3. In vitro polarization study also confirmed the contribution of Foxo1 in microRNA 182 mediated down-regulation of Foxp3+ T cells. Together, our results provide evidence that during the development of EAE, microRNA 182 repressed Treg cells differentiation through the Foxo1 dependent pathway.
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microRNA 182 inhibits CD4+CD25+Foxp3+ Treg differentiation in experimental autoimmune encephalomyelitis.
Clinical Immunology, 2016Co-Authors: Changyun Ping, Xiaoyu Shang, Jiangtian Tian, Sihan Zhao, Lei Li, Shaohong Fang, Yanfeng Zhao, Zhaoying LiAbstract:microRNA 182 has been found to have a distinct contribution in the clonal expansion of activated- and functioning of specialized-helper T cells. In this study we knocked down microRNA 182 in vivo and induced experimental autoimmune encephalomyelitis (EAE) to determine the influences of microRNA 182 in the Treg cells functional specialization through Foxo1 dependent pathway in the peripheral lymphoid organs. Down-regulation of microRNA 182 significantly increased the proportions of Foxp3+ T cells in the peripheral lymph nodes and spleen. In vivo study verified a positive correlation between microRNA 182 levels and symptom severity of EAE, and a negative correlation between microRNA 182 and the transcriptional factor Foxp3. In vitro polarization study also confirmed the contribution of Foxo1 in microRNA 182 mediated down-regulation of Foxp3+ T cells. Together, our results provide evidence that during the development of EAE, microRNA 182 repressed Treg cells differentiation through the Foxo1 dependent pathway.