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Chia-ter Chao - One of the best experts on this subject based on the ideXlab platform.
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microRNA-125b in vascular diseases: An updated systematic review of pathogenetic implications and clinical applications
Journal of cellular and molecular medicine, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Chih-kang Chiang, Huei-wen ChenAbstract:Epigenetic changes, particularly non-coding RNAs, have been implicated extensively in the pathogenesis of vascular diseases. Specific miRNAs are involved in the differentiation, phenotypic switch, proliferation, apoptosis, cytokine production and matrix deposition of endothelial cells and/or vascular smooth muscle cells. microRNA-125b has been studied in depth for its role in carcinogenesis with a double-edged role; that is, it can act as an oncogene in some cancer types and as a tumour suppressor gene in others. However, cumulative evidence from the use of advanced miRNA profiling techniques and bioinformatics analysis suggests that miR-125b can be a potential mediator and useful marker of vascular diseases. Currently, the exact role of miR-125b in vascular diseases is not known. In this systematic review, we intend to provide an updated compilation of all the recent findings of miR-125b in vascular diseases, using a systematic approach of retrieving data from all available reports followed by data summarization. MiR-125b serves as a pathogenic player in multiple vascular pathologies involving endothelia and vascular smooth muscle cells and also serves as a diagnostic marker for vascular diseases. We further provide a computational biologic presentation of the complex network of miR-125b and its target genes within the scope of vascular diseases.
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Risk factors associated with altered circulating microRNA-125b and their influences on uremic vascular calcification among patients with end-stage renal disease
Journal of the American Heart Association, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Hsuan-yu Chen, Jenq-wen Huang, Huei-wen ChenAbstract:Background microRNA‐125b (miR‐125b) has been shown to regulate vascular calcification (VC), and serum miR‐125b levels are a potential biomarker for estimating the risk of uremic VC status. However,...
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Circulating microRNA-125b Predicts the Presence and Progression of Uremic Vascular Calcification
Arteriosclerosis thrombosis and vascular biology, 2017Co-Authors: Chia-ter Chao, Hsiang-yuan Yeh, Hsuan-yu Chen, Jenq-wen Huang, You-pi Liu, Pei-jung Lee, Wan-jiun Chen, Yee-ming Lee, Chih-kang ChiangAbstract:Objective—Vascular calcification (VC) is a major cause of mortality in patients with end-stage renal diseases. Biomarkers to predict the progression of VC early are in urgent demand. Approach and R...
Heather Francis - One of the best experts on this subject based on the ideXlab platform.
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Knockout of secretin receptor reduces biliary damage and liver fibrosis in Mdr2^−/− mice by diminishing senescence of cholangiocytes
Laboratory Investigation, 2018Co-Authors: Tianhao Zhou, Fanyin Meng, Julie Venter, Konstantina Kyritsi, Heather Francis, Antonio Franchitto, Domenico Alvaro, Thao K Giang, Marco Marzioni, Paolo OnoriAbstract:In this study the authors demonstrate that the secretin/secretin receptor axis plays a regulatory role in biliary proliferation and liver fibrosis through differential changes in the senescence of cholangiocytes and hepatic stellate cells in a mouse model of primary sclerosing cholangitis. Targeting senescent cholangiocytes by modulation of the secretin/secretin receptor axis may provide a key therapeutic approach in the treatment of cholestatic liver diseases. Secretin receptor (SR), only expressed by cholangiocytes, plays a key role in the regulation of biliary damage and liver fibrosis. The aim of this study was to determine the effects of genetic depletion of SR in Mdr2^−/− mice on intrahepatic biliary mass, liver fibrosis, senescence, and angiogenesis. 12 wk SR^−/−, Mdr2^−/−, and SR^−/−/Mdr2^−/− mice with corresponding wild-type mice were used for the in vivo studies. Immunohistochemistry or immunofluorescence was performed in liver sections for (i) biliary expression of SR; (ii) hematoxylin and eosin; (iii) intrahepatic biliary mass by CK-19; (iv) fibrosis by Col1a1 and α-SMA; (v) senescence by SA-β-gal and p16; and (vi) angiogenesis by VEGF-A and CD31. Secretin (Sct) and TGF-β1 levels were measured in serum and cholangiocyte supernatant by ELISA. In total liver, isolated cholangiocytes or HSCs, we evaluated the expression of fibrosis markers (FN-1 and Col1a1); senescence markers (p16 and CCL2); microRNA 125b and angiogenesis markers (VEGF-A, VEGFR-2, CD31, and vWF) by immunoblots and/or qPCR. In vitro, we measured the paracrine effect of cholangiocyte supernatant on the expression of senescent and fibrosis markers in human hepatic stellate cells (HHSteCs). The increased level of ductular reaction, fibrosis, and angiogenesis in Mdr2^−/− mice was reduced in SR^−/−/Mdr2^−/− mice. Enhanced senescence levels in cholangiocytes from Mdr2^−/− mice were reversed to normal in SR^−/−/Mdr2^−/− mice. However, senescence was decreased in HSCs from Mdr2^−/− mice but returned to normal values in SR^−/−/Mdr2^−/− mice. In vitro treatment of HHSteCs with supernatant from cholangiocyte lacking SR (containing lower biliary levels of Sct-dependent TGF-β1) have decreased fibrotic reaction and increased cellular senescence. Sct-induced TGF-β1 secretion was mediated by microRNA 125b. Our data suggest that differential modulation of angiogenesis-dependent senescence of cholangiocytes and HSCs may be important for the treatment of liver fibrosis in cholangiopathies.
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knockout of secretin receptor reduces biliary damage and liver fibrosis in mdr2 mice by diminishing senescence of cholangiocytes
Laboratory Investigation, 2018Co-Authors: Tianhao Zhou, Fanyin Meng, Julie Venter, Konstantina Kyritsi, Heather Francis, Thao Giang, Antonio FranchittoAbstract:Secretin receptor (SR), only expressed by cholangiocytes, plays a key role in the regulation of biliary damage and liver fibrosis. The aim of this study was to determine the effects of genetic depletion of SR in Mdr2−/− mice on intrahepatic biliary mass, liver fibrosis, senescence, and angiogenesis. 12 wk SR−/−, Mdr2−/−, and SR−/−/Mdr2−/− mice with corresponding wild-type mice were used for the in vivo studies. Immunohistochemistry or immunofluorescence was performed in liver sections for (i) biliary expression of SR; (ii) hematoxylin and eosin; (iii) intrahepatic biliary mass by CK-19; (iv) fibrosis by Col1a1 and α-SMA; (v) senescence by SA-β-gal and p16; and (vi) angiogenesis by VEGF-A and CD31. Secretin (Sct) and TGF-β1 levels were measured in serum and cholangiocyte supernatant by ELISA. In total liver, isolated cholangiocytes or HSCs, we evaluated the expression of fibrosis markers (FN-1 and Col1a1); senescence markers (p16 and CCL2); microRNA 125b and angiogenesis markers (VEGF-A, VEGFR-2, CD31, and vWF) by immunoblots and/or qPCR. In vitro, we measured the paracrine effect of cholangiocyte supernatant on the expression of senescent and fibrosis markers in human hepatic stellate cells (HHSteCs). The increased level of ductular reaction, fibrosis, and angiogenesis in Mdr2−/− mice was reduced in SR−/−/Mdr2−/− mice. Enhanced senescence levels in cholangiocytes from Mdr2−/− mice were reversed to normal in SR−/−/Mdr2−/− mice. However, senescence was decreased in HSCs from Mdr2−/− mice but returned to normal values in SR−/−/Mdr2−/− mice. In vitro treatment of HHSteCs with supernatant from cholangiocyte lacking SR (containing lower biliary levels of Sct-dependent TGF-β1) have decreased fibrotic reaction and increased cellular senescence. Sct-induced TGF-β1 secretion was mediated by microRNA 125b. Our data suggest that differential modulation of angiogenesis-dependent senescence of cholangiocytes and HSCs may be important for the treatment of liver fibrosis in cholangiopathies.
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secretin stimulates biliary cell proliferation by regulating expression of microRNA 125b and microRNA let7a in mice
Gastroenterology, 2014Co-Authors: Fanyin Meng, Julie Venter, Heather Francis, Paolo Onori, Shannon Glaser, Yuyan Han, Billy K C Chow, Kelly McdanielAbstract:Background & Aims Proliferating cholangiocytes secrete and respond to neuroendocrine hormones, including secretin. We investigated whether secretin secreted by S cells and cholangiocytes stimulates biliary proliferation in mice. Methods Cholestasis was induced in secretin knockout ( Sct −/− ) and wild-type (control) mice by bile duct ligation (BDL). At days 3 and 7 after BDL, control and Sct −/− mice received tail-vein injections of morpholinos against microRNA 125b or let7a. One week later, liver tissues and cholangiocytes were collected. Immunohistochemical, immunoblot, luciferase reporter, and real-time polymerase chain reaction assays were performed. Intrahepatic bile duct mass (IBDM) and proliferation were measured. Secretin secretion was measured in conditioned media from cholangiocytes and S cells and in serum and bile. Results Secretin secretion was increased in supernatants from cholangiocytes and S cells and in serum and bile after BDL in control mice. BDL Sct −/− mice had lower IBDM, reduced proliferation, and reduced production of vascular endothelial growth factor (VEGF) A and nerve growth factor (NGF) compared with BDL control. BDL and control mice given morpholinos against microRNA 125b or let7a had increased IBDM. Livers of mice given morpholinos against microRNA 125b had increased expression of VEGFA, and those treated with morpholinos against microRNA let7a had increased expression of NGF. Secretin regulated VEGF and NGF expression that negatively correlated with microRNA 125b and let7a levels in liver tissue. Conclusions After liver injury, secretin produced by cholangiocytes and S cells reduces microRNA 125b and let7a levels, resulting in up-regulation of VEGF and NGF. Modulation of cholangiocyte expression of secretin could be a therapeutic approach for biliary diseases.
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Regulation of placenta growth factor by microRNA-125b in hepatocellular cancer.
Journal of hepatology, 2011Co-Authors: Gianfranco Alpini, Heather Francis, Shannon Glaser, Yuyan Han, Jing Ping Zhang, Jiao Gong, Allison Stokes, Taylor Francis, Nathan Hughart, Levi HubbleAbstract:Background & Aims microRNAs (miRNAs) are a class of small noncoding RNAs that can regulate gene expression by translation repression or mRNA degradation. Our aim was to evaluate the role of aberrantly expressed miRNAs in hepatocellular cancer (HCC). Methods miRNA expression in HCC tissues and cells was evaluated by qPCR array and Taqman miRNA assay. Cell proliferation, motility, invasion, and the angiogenesis index were quantitated using commercial assays. DNA methylation status, matrix metalloproteinases (MMPs) mRNA expression was quantitated by real-time PCR analysis. Results miRNA profiling identified a decrease in miR-125b expression in HCC tumor tissues and cell lines. The expression of miR-125b was significantly increased by the methylation inhibitor 5-aza-2′-deoxycytidine in HCC cells but not in normal controls, suggesting that the expression of miR-125b could be epigenetically modulated. Methylation-specific PCR revealed hypermethylation status of miR-125b in HCC cells compared to non-malignant controls. Cell proliferation, anchorage-independent growth, cell migration, invasion, and angiogenesis were significantly decreased by the introduction of miR-125b precursor in HCC cell lines. Placenta growth factor was identified as a target of miR-125b by bioinformatics analysis and experimentally verified using luciferase reporter constructs. Overexpression of miR-125b in HCC cells decreased PIGF expression, and altered the angiogenesis index. Furthermore, modulation of miR-125b also distorted expression of MMP-2 and -9, the mediators of enzymatic degradation of the extracellular matrix. Conclusions Our studies showing epigenetic silencing of miR-125b contributes to an invasive phenotype provide novel mechanistic insights and identify a potential target mechanism that could be manipulated for therapeutic benefit in HCC.
David L. Williams - One of the best experts on this subject based on the ideXlab platform.
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microRNA-125b Prevents Cardiac Dysfunction in Polymicrobial Sepsis by Targeting TRAF6-Mediated Nuclear Factor κB Activation and p53-Mediated Apoptotic Signaling
The Journal of infectious diseases, 2016Co-Authors: Xiaohui Wang, Li Liu, John Kalbfleisch, Ming Gao, Ruitao Wang, Race L. Kao, David L. WilliamsAbstract:BACKGROUND This study examined the effect of microRNA-125b (miR-125b) on sepsis-induced cardiac dysfunction. METHODS Mouse hearts were transfected with lentivirus expressing miR-125b (LmiR-125b) 7 days before cecal ligation and puncture (CLP)-induced sepsis. Cardiac function was examined by echocardiography before and 6 hours after CLP (n = 6/group). Survival was monitored following CLP-induced sepsis (n = 12/group). RESULTS LmiR-125b transfection significantly attenuated cardiac dysfunction due to CLP-induced sepsis. Fractional shortening and ejection fraction values were significantly (P < .05) higher in the LmiR-125b-treated CLP group than in the untreated CLP group. Survival outcome in LmiR-125b-transfected septic mice was markedly improved, compared with mice with CLP-induced sepsis. Transfection of LmiR-125b into the heart significantly suppressed the expression of ICAM-1 and VCAM-1, decreased the accumulation of macrophages and neutrophils in the myocardium, and decreased serum levels of tumor necrosis factor α and interleukin 1β by targeting tumor necrosis factor receptor-associated factor 6 (TRAF6)-mediated nuclear factor κB (NF-κB) activation. In addition, sepsis-induced myocardial apoptosis was markedly attenuated by LmiR-125b transfection through suppression of p53, Bax, and Bak1 expression. In vitro transfection of endothelial cells with miR-125b mimics attenuate LPS-induced ICAM-1 and VCAM-1 expression by suppressing TRAF6 and NF-κB activation. CONCLUSIONS Increased myocardial miR-125b expression attenuates sepsis-induced cardiac dysfunction and improves survival. miR-125b may be a target for septic cardiomyopathy.
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microRNA 125b protects against myocardial ischaemia reperfusion injury via targeting p53 mediated apoptotic signalling and traf6
Cardiovascular Research, 2014Co-Authors: Xiaohui Wang, Jianghuan Zou, Danyang Ren, Li Liu, Xia Zhang, John Kalbfleisch, Xiang Gao, David L. WilliamsAbstract:Aims The present study examined the role of microRNA-125b (miR-125b) in myocardial ischaemia/reperfusion (I/R) injury. We constructed lentivirus-expressing miR-125b (LmiR-125b) and developed transgenic mice with overexpression of miR-125b. Methods and results LmiR-125b was transfected into mouse hearts through the right common carotid artery. Lentivirus vector (LmiR-Con) served as vector control. Untreated mice served as I/R control. Sham operation served as sham control. Seven days after transfection, the hearts were subjected to ischaemia (45 min) followed by reperfusion (4 h). Myocardial infarct size was analysed by 2,3,5-triphenyltetrazolium chloride staining. In separate experiments, hearts were subjected to ischaemia (45 min) followed by reperfusion for up to 7 days. Cardiac function was measured by echocardiography before, as well as 3 and 7 days after myocardial I/R. Increased expression of miR-125b significantly decreased I/R-induced myocardial infarct size by 60% and prevented I/R-induced decreases in ejection fraction (EF%) and fractional shortening (%FS). Transgenic mice with overexpression of miR-125b also showed the protection against myocardial I/R injury. Increased expression of miR-125b attenuated I/R-induced myocardial apoptosis and caspase-3/7 and -8 activities. Western blot showed that increased expression of miR-125b suppresses p53 and Bak1 expression in the myocardium. In addition, transfection of LmiR-125b decreased the levels of TNF receptor-associated factor 6 (TRAF6) and prevented I/R-induced NF-κB activation. Conclusion miR-125 protects the myocardium from I/R injury by preventing p53-mediated apoptotic signalling and suppressing TRAF6-mediated NF-κB activation.
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microRNA-125b protects against myocardial ischaemia/reperfusion injury via targeting p53-mediated apoptotic signalling and TRAF6.
Cardiovascular research, 2014Co-Authors: Xiaohui Wang, Jianghuan Zou, Danyang Ren, Li Liu, Xia Zhang, John Kalbfleisch, Xiang Gao, David L. WilliamsAbstract:Aims The present study examined the role of microRNA-125b (miR-125b) in myocardial ischaemia/reperfusion (I/R) injury. We constructed lentivirus-expressing miR-125b (LmiR-125b) and developed transgenic mice with overexpression of miR-125b. Methods and results LmiR-125b was transfected into mouse hearts through the right common carotid artery. Lentivirus vector (LmiR-Con) served as vector control. Untreated mice served as I/R control. Sham operation served as sham control. Seven days after transfection, the hearts were subjected to ischaemia (45 min) followed by reperfusion (4 h). Myocardial infarct size was analysed by 2,3,5-triphenyltetrazolium chloride staining. In separate experiments, hearts were subjected to ischaemia (45 min) followed by reperfusion for up to 7 days. Cardiac function was measured by echocardiography before, as well as 3 and 7 days after myocardial I/R. Increased expression of miR-125b significantly decreased I/R-induced myocardial infarct size by 60% and prevented I/R-induced decreases in ejection fraction (EF%) and fractional shortening (%FS). Transgenic mice with overexpression of miR-125b also showed the protection against myocardial I/R injury. Increased expression of miR-125b attenuated I/R-induced myocardial apoptosis and caspase-3/7 and -8 activities. Western blot showed that increased expression of miR-125b suppresses p53 and Bak1 expression in the myocardium. In addition, transfection of LmiR-125b decreased the levels of TNF receptor-associated factor 6 (TRAF6) and prevented I/R-induced NF-κB activation. Conclusion miR-125 protects the myocardium from I/R injury by preventing p53-mediated apoptotic signalling and suppressing TRAF6-mediated NF-κB activation.
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sr a deficiency reduces myocardial ischemia reperfusion injury involvement of increased microRNA 125b expression in macrophages
Biochimica et Biophysica Acta, 2013Co-Authors: Danyang Ren, Xiaohui Wang, Li Liu, John Kalbfleisch, Xiang Gao, David L. WilliamsAbstract:Abstract The macrophage scavenger receptor class A (SR-A) participates in the innate immune and inflammatory responses. This study examined the role of macrophage SR-A in myocardial ischemia/reperfusion (I/R) injury and hypoxia/reoxygenation (H/R)-induced cell damage. SR-A −/− and WT mice were subjected to ischemia (45 min) followed by reperfusion for up to 7 days. SR-A −/− mice showed smaller myocardial infarct size and better cardiac function than did WT I/R mice. SR-A deficiency attenuated I/R-induced myocardial apoptosis by preventing p53-mediated Bak-1 apoptotic signaling. The levels of microRNA-125b in SR-A −/− heart were significantly greater than in WT myocardium. SR-A is predominantly expressed on macrophages. To investigate the role of SR-A macrophages in H/R-induced injury, we isolated peritoneal macrophages from SR-A deficient (SR-A −/− ) and wild type (WT) mice. Macrophages were subjected to hypoxia followed by reoxygenation. H/R markedly increased NF-κB binding activity as well as KC and MCP-1 production in WT macrophages but not in SR-A −/− macrophages. H/R induced caspase-3/7 and -8 activities and cell death in WT macrophages, but not in SR-A −/− macrophages. The levels of miR-125b in SR-A −/− macrophages were significantly higher than in WT macrophages. Transfection of WT macrophages with miR-125b mimics attenuated H/R-induced caspase-3/7 and -8 activities and H/R-decreased viability, and prevented H/R-increased p-53, Bak-1 and Bax expression. The data suggest that SR-A deficiency attenuates myocardial I/R injury by targeting p53-mediated apoptotic signaling. SR-A −/− macrophages contain high levels of miR-125b which may play a role in the protective effect of SR-A deficiency on myocardial I/R injury and H/R-induced cell damage.
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SR-A deficiency reduces myocardial ischemia/reperfusion injury; involvement of increased microRNA-125b expression in macrophages.
Biochimica et biophysica acta, 2012Co-Authors: Danyang Ren, Xiaohui Wang, Li Liu, John Kalbfleisch, Xiang Gao, David L. WilliamsAbstract:Abstract The macrophage scavenger receptor class A (SR-A) participates in the innate immune and inflammatory responses. This study examined the role of macrophage SR-A in myocardial ischemia/reperfusion (I/R) injury and hypoxia/reoxygenation (H/R)-induced cell damage. SR-A −/− and WT mice were subjected to ischemia (45 min) followed by reperfusion for up to 7 days. SR-A −/− mice showed smaller myocardial infarct size and better cardiac function than did WT I/R mice. SR-A deficiency attenuated I/R-induced myocardial apoptosis by preventing p53-mediated Bak-1 apoptotic signaling. The levels of microRNA-125b in SR-A −/− heart were significantly greater than in WT myocardium. SR-A is predominantly expressed on macrophages. To investigate the role of SR-A macrophages in H/R-induced injury, we isolated peritoneal macrophages from SR-A deficient (SR-A −/− ) and wild type (WT) mice. Macrophages were subjected to hypoxia followed by reoxygenation. H/R markedly increased NF-κB binding activity as well as KC and MCP-1 production in WT macrophages but not in SR-A −/− macrophages. H/R induced caspase-3/7 and -8 activities and cell death in WT macrophages, but not in SR-A −/− macrophages. The levels of miR-125b in SR-A −/− macrophages were significantly higher than in WT macrophages. Transfection of WT macrophages with miR-125b mimics attenuated H/R-induced caspase-3/7 and -8 activities and H/R-decreased viability, and prevented H/R-increased p-53, Bak-1 and Bax expression. The data suggest that SR-A deficiency attenuates myocardial I/R injury by targeting p53-mediated apoptotic signaling. SR-A −/− macrophages contain high levels of miR-125b which may play a role in the protective effect of SR-A deficiency on myocardial I/R injury and H/R-induced cell damage.
Huei-wen Chen - One of the best experts on this subject based on the ideXlab platform.
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microRNA-125b in vascular diseases: An updated systematic review of pathogenetic implications and clinical applications
Journal of cellular and molecular medicine, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Chih-kang Chiang, Huei-wen ChenAbstract:Epigenetic changes, particularly non-coding RNAs, have been implicated extensively in the pathogenesis of vascular diseases. Specific miRNAs are involved in the differentiation, phenotypic switch, proliferation, apoptosis, cytokine production and matrix deposition of endothelial cells and/or vascular smooth muscle cells. microRNA-125b has been studied in depth for its role in carcinogenesis with a double-edged role; that is, it can act as an oncogene in some cancer types and as a tumour suppressor gene in others. However, cumulative evidence from the use of advanced miRNA profiling techniques and bioinformatics analysis suggests that miR-125b can be a potential mediator and useful marker of vascular diseases. Currently, the exact role of miR-125b in vascular diseases is not known. In this systematic review, we intend to provide an updated compilation of all the recent findings of miR-125b in vascular diseases, using a systematic approach of retrieving data from all available reports followed by data summarization. MiR-125b serves as a pathogenic player in multiple vascular pathologies involving endothelia and vascular smooth muscle cells and also serves as a diagnostic marker for vascular diseases. We further provide a computational biologic presentation of the complex network of miR-125b and its target genes within the scope of vascular diseases.
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Risk factors associated with altered circulating microRNA-125b and their influences on uremic vascular calcification among patients with end-stage renal disease
Journal of the American Heart Association, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Hsuan-yu Chen, Jenq-wen Huang, Huei-wen ChenAbstract:Background microRNA‐125b (miR‐125b) has been shown to regulate vascular calcification (VC), and serum miR‐125b levels are a potential biomarker for estimating the risk of uremic VC status. However,...
Hsiang-yuan Yeh - One of the best experts on this subject based on the ideXlab platform.
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microRNA-125b in vascular diseases: An updated systematic review of pathogenetic implications and clinical applications
Journal of cellular and molecular medicine, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Chih-kang Chiang, Huei-wen ChenAbstract:Epigenetic changes, particularly non-coding RNAs, have been implicated extensively in the pathogenesis of vascular diseases. Specific miRNAs are involved in the differentiation, phenotypic switch, proliferation, apoptosis, cytokine production and matrix deposition of endothelial cells and/or vascular smooth muscle cells. microRNA-125b has been studied in depth for its role in carcinogenesis with a double-edged role; that is, it can act as an oncogene in some cancer types and as a tumour suppressor gene in others. However, cumulative evidence from the use of advanced miRNA profiling techniques and bioinformatics analysis suggests that miR-125b can be a potential mediator and useful marker of vascular diseases. Currently, the exact role of miR-125b in vascular diseases is not known. In this systematic review, we intend to provide an updated compilation of all the recent findings of miR-125b in vascular diseases, using a systematic approach of retrieving data from all available reports followed by data summarization. MiR-125b serves as a pathogenic player in multiple vascular pathologies involving endothelia and vascular smooth muscle cells and also serves as a diagnostic marker for vascular diseases. We further provide a computational biologic presentation of the complex network of miR-125b and its target genes within the scope of vascular diseases.
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Risk factors associated with altered circulating microRNA-125b and their influences on uremic vascular calcification among patients with end-stage renal disease
Journal of the American Heart Association, 2019Co-Authors: Chia-ter Chao, Tzu-hang Yuan, Hsiang-yuan Yeh, Hsuan-yu Chen, Jenq-wen Huang, Huei-wen ChenAbstract:Background microRNA‐125b (miR‐125b) has been shown to regulate vascular calcification (VC), and serum miR‐125b levels are a potential biomarker for estimating the risk of uremic VC status. However,...
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Circulating microRNA-125b Predicts the Presence and Progression of Uremic Vascular Calcification
Arteriosclerosis thrombosis and vascular biology, 2017Co-Authors: Chia-ter Chao, Hsiang-yuan Yeh, Hsuan-yu Chen, Jenq-wen Huang, You-pi Liu, Pei-jung Lee, Wan-jiun Chen, Yee-ming Lee, Chih-kang ChiangAbstract:Objective—Vascular calcification (VC) is a major cause of mortality in patients with end-stage renal diseases. Biomarkers to predict the progression of VC early are in urgent demand. Approach and R...