The Experts below are selected from a list of 89253 Experts worldwide ranked by ideXlab platform

Nitai P. Bhattacharyya - One of the best experts on this subject based on the ideXlab platform.

  • microRNA 124 targets ccna2 and regulates cell cycle in sthdhq111 hdhq111 cells
    Biochemical and Biophysical Research Communications, 2013
    Co-Authors: Eashita Das, Nihar Ranjan Jana, Nitai P. Bhattacharyya
    Abstract:

    Mutation in huntingtin (HTT) gene causes Huntington’s disease (HD). Expression of many micro RNAs is known to alter in cell, animal models and brains of HD patients, but their cellular effects are not known. Here, we show that expression of microRNA-124 (miR-124) is down regulated in HD striatal mutant STHdhQ111/HdhQ111 cells, a cell model of HD compared to STHdhQ7/HdhQ7 cells. STHdhQ7/HdhQ7 and STHdhQ111/HdhQ111 cells express endogenously full length wild type and mutant HTT respectively. We confirmed this result in R6/2 mouse, an animal model of HD, expressing mutant HTT. Gene Ontology terms related to cell cycle were enriched significantly with experimentally validated targets of miR-124. We observed that expression of Cyclin A2 (CCNA2), a putative target of miR-124 was increased in mutant STHdhQ111/HdhQ111 cells and brains of R6/2 mice. Fraction of cells in S phase was higher in asynchronously growing mutant STHdhQ111/HdhQ111 cells compared to wild type STHdhQ7/HdhQ7 cells and could be altered by exogenous expression or inhibition of miR-124. Exogenous expression or knock down of CCNA2, a target of miR-124, also alters proportion of cells in S phase of HD cell model. In summary, decreased miR-124 expression could increase CCNA2 in cell and animal model of HD and is involved in deregulation of cell cycle in STHdhQ111/HdhQ111 cells.

  • microRNA-124 targets CCNA2 and regulates cell cycle in STHdhQ111/HdhQ111 cells
    Biochemical and biophysical research communications, 2013
    Co-Authors: Eashita Das, Nihar Ranjan Jana, Nitai P. Bhattacharyya
    Abstract:

    Mutation in huntingtin (HTT) gene causes Huntington’s disease (HD). Expression of many micro RNAs is known to alter in cell, animal models and brains of HD patients, but their cellular effects are not known. Here, we show that expression of microRNA-124 (miR-124) is down regulated in HD striatal mutant STHdhQ111/HdhQ111 cells, a cell model of HD compared to STHdhQ7/HdhQ7 cells. STHdhQ7/HdhQ7 and STHdhQ111/HdhQ111 cells express endogenously full length wild type and mutant HTT respectively. We confirmed this result in R6/2 mouse, an animal model of HD, expressing mutant HTT. Gene Ontology terms related to cell cycle were enriched significantly with experimentally validated targets of miR-124. We observed that expression of Cyclin A2 (CCNA2), a putative target of miR-124 was increased in mutant STHdhQ111/HdhQ111 cells and brains of R6/2 mice. Fraction of cells in S phase was higher in asynchronously growing mutant STHdhQ111/HdhQ111 cells compared to wild type STHdhQ7/HdhQ7 cells and could be altered by exogenous expression or inhibition of miR-124. Exogenous expression or knock down of CCNA2, a target of miR-124, also alters proportion of cells in S phase of HD cell model. In summary, decreased miR-124 expression could increase CCNA2 in cell and animal model of HD and is involved in deregulation of cell cycle in STHdhQ111/HdhQ111 cells.

Hui Zhang - One of the best experts on this subject based on the ideXlab platform.

  • identification of microRNA 124 as a major regulator of enhanced endothelial cell glycolysis in pulmonary arterial hypertension via ptbp1 polypyrimidine tract binding protein and pyruvate kinase m2
    Circulation, 2017
    Co-Authors: Paola Caruso, Hui Zhang, Benjamin J Dunmore, Kenny Schlosser, Sandra Schoors, Claudia Dos Santos, Carol Pereziratxeta, J R Lavoie, Lu Long, Amanda Flockton
    Abstract:

    Background:Pulmonary arterial hypertension (PAH) is characterized by abnormal growth and enhanced glycolysis of pulmonary artery endothelial cells. However, the mechanisms underlying alterations in energy production have not been identified. Methods:Here, we examined the miRNA and proteomic profiles of blood outgrowth endothelial cells (BOECs) from patients with heritable PAH caused by mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene and patients with idiopathic PAH to determine mechanisms underlying abnormal endothelial glycolysis. We hypothesized that in BOECs from patients with PAH, the downregulation of microRNA-124 (miR-124), determined with a tiered systems biology approach, is responsible for increased expression of the splicing factor PTBP1 (polypyrimidine tract binding protein), resulting in alternative splicing of pyruvate kinase muscle isoforms 1 and 2 (PKM1 and 2) and consequently increased PKM2 expression. We questioned whether this alternative regulation plays a criti...

  • loss of microRNA 124 expression in neurons in the peri lesion area in mice with spinal cord injury
    Neural Regeneration Research, 2015
    Co-Authors: Yu Zhao, Hui Zhang, Dan Zhang, Xianghui Zhao, Fangfang Liu, Ganlan Bian, Jian Wang
    Abstract:

    microRNA-124 (miR-124) is abundantly expressed in neurons in the mammalian central nervous system, and plays critical roles in the regulation of gene expression during embryonic neurogenesis and postnatal neural differentiation. However, the expression profile of miR-124 after spinal cord injury and the underlying regulatory mechanisms are not well understood. In the present study, we examined the expression of miR-124 in mouse brain and spinal cord after spinal cord injury using in situ hybridization. Furthermore, the expression of miR-124 was examined with quantitative RT-PCR at 1, 3 and 7 days after spinal cord injury. The miR-124 expression in neurons at the site of injury was evaluated by in situ hybridization combined with NeuN immunohistochemical staining. The miR-124 was mainly expressed in neurons throughout the brain and spinal cord. The expression of miR-124 in neurons significantly decreased within 7 days after spinal cord injury. Some of the neurons in the peri-lesion area were NeuN(+)/miR-124(-). Moreover, the neurons distal to the peri-lesion site were NeuN(+)/miR-124(+). These findings indicate that miR-124 expression in neurons is reduced after spinal cord injury, and may reflect the severity of spinal cord injury.

  • microRNA-124 Controls the Proliferative, Migratory, and Inflammatory Phenotype of Pulmonary Vascular Fibroblasts
    Circulation research, 2013
    Co-Authors: Daren Wang, Hui Zhang, Maria G. Frid, Amanda Flockton, B. Alexandre Mckeon, Michael E. Yeager, Mehdi A. Fini, Nicholas W. Morrell, Soni Savai Pullamsetti
    Abstract:

    Rationale:Pulmonary hypertensive remodeling is characterized by excessive proliferation, migration, and proinflammatory activation of adventitial fibroblasts. In culture, fibroblasts maintain a similar activated phenotype. The mechanisms responsible for generation/maintenance of this phenotype remain unknown. Objective:We hypothesized that aberrant expression of microRNA-124 (miR-124) regulates this activated fibroblast phenotype and sought to determine the signaling pathways through which miR-124 exerts effects. Methods and Results:We detected significant decreases in miR-124 expression in fibroblasts isolated from calves and humans with severe pulmonary hypertension. Overexpression of miR-124 by mimic transfection significantly attenuated proliferation, migration, and monocyte chemotactic protein-1 expression of hypertensive fibroblasts, whereas anti–miR-124 treatment of control fibroblasts resulted in their increased proliferation, migration, and monocyte chemotactic protein-1 expression. Furthermore, ...

Eashita Das - One of the best experts on this subject based on the ideXlab platform.

  • microRNA 124 targets ccna2 and regulates cell cycle in sthdhq111 hdhq111 cells
    Biochemical and Biophysical Research Communications, 2013
    Co-Authors: Eashita Das, Nihar Ranjan Jana, Nitai P. Bhattacharyya
    Abstract:

    Mutation in huntingtin (HTT) gene causes Huntington’s disease (HD). Expression of many micro RNAs is known to alter in cell, animal models and brains of HD patients, but their cellular effects are not known. Here, we show that expression of microRNA-124 (miR-124) is down regulated in HD striatal mutant STHdhQ111/HdhQ111 cells, a cell model of HD compared to STHdhQ7/HdhQ7 cells. STHdhQ7/HdhQ7 and STHdhQ111/HdhQ111 cells express endogenously full length wild type and mutant HTT respectively. We confirmed this result in R6/2 mouse, an animal model of HD, expressing mutant HTT. Gene Ontology terms related to cell cycle were enriched significantly with experimentally validated targets of miR-124. We observed that expression of Cyclin A2 (CCNA2), a putative target of miR-124 was increased in mutant STHdhQ111/HdhQ111 cells and brains of R6/2 mice. Fraction of cells in S phase was higher in asynchronously growing mutant STHdhQ111/HdhQ111 cells compared to wild type STHdhQ7/HdhQ7 cells and could be altered by exogenous expression or inhibition of miR-124. Exogenous expression or knock down of CCNA2, a target of miR-124, also alters proportion of cells in S phase of HD cell model. In summary, decreased miR-124 expression could increase CCNA2 in cell and animal model of HD and is involved in deregulation of cell cycle in STHdhQ111/HdhQ111 cells.

  • microRNA-124 targets CCNA2 and regulates cell cycle in STHdhQ111/HdhQ111 cells
    Biochemical and biophysical research communications, 2013
    Co-Authors: Eashita Das, Nihar Ranjan Jana, Nitai P. Bhattacharyya
    Abstract:

    Mutation in huntingtin (HTT) gene causes Huntington’s disease (HD). Expression of many micro RNAs is known to alter in cell, animal models and brains of HD patients, but their cellular effects are not known. Here, we show that expression of microRNA-124 (miR-124) is down regulated in HD striatal mutant STHdhQ111/HdhQ111 cells, a cell model of HD compared to STHdhQ7/HdhQ7 cells. STHdhQ7/HdhQ7 and STHdhQ111/HdhQ111 cells express endogenously full length wild type and mutant HTT respectively. We confirmed this result in R6/2 mouse, an animal model of HD, expressing mutant HTT. Gene Ontology terms related to cell cycle were enriched significantly with experimentally validated targets of miR-124. We observed that expression of Cyclin A2 (CCNA2), a putative target of miR-124 was increased in mutant STHdhQ111/HdhQ111 cells and brains of R6/2 mice. Fraction of cells in S phase was higher in asynchronously growing mutant STHdhQ111/HdhQ111 cells compared to wild type STHdhQ7/HdhQ7 cells and could be altered by exogenous expression or inhibition of miR-124. Exogenous expression or knock down of CCNA2, a target of miR-124, also alters proportion of cells in S phase of HD cell model. In summary, decreased miR-124 expression could increase CCNA2 in cell and animal model of HD and is involved in deregulation of cell cycle in STHdhQ111/HdhQ111 cells.

Javid Sabour Takanlu - One of the best experts on this subject based on the ideXlab platform.

  • indirect tumor inhibitory effects of microRNA 124 through targeting ezh2 in the multiple myeloma cell line
    Cell, 2020
    Co-Authors: S Abroun, Javid Sabour Takanlu, Arad Aghaie Fard, Saeed Mohammdi, Mohsen Nikbakht
    Abstract:

    Objective: Multiple myeloma (MM) is an incurable plasma cell malignancy. Several genetic and epigenetic changes affect numerous critical genes expression status in this disorder. CDKN2A gene is expressed at low level in almost all cases with MM disease. The mechanism of this gene down-regulation has remained controversial. In the present study, we targeted EZH2 by microRNA-124 (miR-124) in L-363 cells and assessed following possible impact on CDKN2A gene expression and phenotypic changes. Materials and Methods: In this experimental study, growth inhibitory effects of miR-124 were measured by MTT assay in L-363 cell line. Likewise, cell cycle assay was measured by flowcytometery. The expression levels of EZH2 and CDKN2A were evaluated by real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Results: qRT-PCR results showed induction of EZH2 gene expression after transduction of cells with lentivector expressing miR-124. The expression of CDKN2A was also upregulated as the result of EZH2 supression. Coincide with gene expression changes, cell cycle analysis by flow-cytometry indicated slightly increased G1-arrest in miRtransduced cells (P<0.05). MTT assay results also showed a significant decrease in viability and proliferation of miRtransduced cells (P<0.05). Conclusion: It seems that assembling of H3K27me3 mark mediated by EZH2 is one of the key mechanisms of suppressing CDKN2A gene expression in MM disease. However, this suppressive function is applied by a multi-factor mechanism. In other words, targeting EZH2, as the core functional subunit of PRC2 complex, can increase expression of the downstream suppressive genes. Consequently, by increasing expression of tumor suppressor genes, myeloma cells are stopped from aberrant expansions and they become susceptible to regulated cellular death.

Mohsen Nikbakht - One of the best experts on this subject based on the ideXlab platform.

  • indirect tumor inhibitory effects of microRNA 124 through targeting ezh2 in the multiple myeloma cell line
    Cell, 2020
    Co-Authors: S Abroun, Javid Sabour Takanlu, Arad Aghaie Fard, Saeed Mohammdi, Mohsen Nikbakht
    Abstract:

    Objective: Multiple myeloma (MM) is an incurable plasma cell malignancy. Several genetic and epigenetic changes affect numerous critical genes expression status in this disorder. CDKN2A gene is expressed at low level in almost all cases with MM disease. The mechanism of this gene down-regulation has remained controversial. In the present study, we targeted EZH2 by microRNA-124 (miR-124) in L-363 cells and assessed following possible impact on CDKN2A gene expression and phenotypic changes. Materials and Methods: In this experimental study, growth inhibitory effects of miR-124 were measured by MTT assay in L-363 cell line. Likewise, cell cycle assay was measured by flowcytometery. The expression levels of EZH2 and CDKN2A were evaluated by real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Results: qRT-PCR results showed induction of EZH2 gene expression after transduction of cells with lentivector expressing miR-124. The expression of CDKN2A was also upregulated as the result of EZH2 supression. Coincide with gene expression changes, cell cycle analysis by flow-cytometry indicated slightly increased G1-arrest in miRtransduced cells (P<0.05). MTT assay results also showed a significant decrease in viability and proliferation of miRtransduced cells (P<0.05). Conclusion: It seems that assembling of H3K27me3 mark mediated by EZH2 is one of the key mechanisms of suppressing CDKN2A gene expression in MM disease. However, this suppressive function is applied by a multi-factor mechanism. In other words, targeting EZH2, as the core functional subunit of PRC2 complex, can increase expression of the downstream suppressive genes. Consequently, by increasing expression of tumor suppressor genes, myeloma cells are stopped from aberrant expansions and they become susceptible to regulated cellular death.

  • Indirect Tumor Inhibitory Effects of microRNA-124 through Targeting EZH2 in The Multiple Myeloma Cell Line.
    Cell journal, 2019
    Co-Authors: Sabour Takanlu J, Aghaie Fard A, Mohammdi S, Hosseini Rad Sma, S Abroun, Mohsen Nikbakht
    Abstract:

    Objective Multiple myeloma (MM) is an incurable plasma cell malignancy. Several genetic and epigenetic changes affect numerous critical genes expression status in this disorder. CDKN2A gene is expressed at low level in almost all cases with MM disease. The mechanism of this gene down-regulation has remained controversial. In the present study, we targeted EZH2 by microRNA-124 (miR-124) in L-363 cells and assessed following possible impact on CDKN2A gene expression and phenotypic changes. Materials and Methods In this experimental study, growth inhibitory effects of miR-124 were measured by MTT assay in L-363 cell line. Likewise, cell cycle assay was measured by flowcytometery. The expression levels of EZH2 and CDKN2A were evaluated by real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Results qRT-PCR results showed induction of EZH2 gene expression after transduction of cells with lentivector expressing miR-124. The expression of CDKN2A was also upregulated as the result of EZH2 supression. Coincide with gene expression changes, cell cycle analysis by flow-cytometry indicated slightly increased G1-arrest in miRtransduced cells (P