13 results on '"Zarghami N"'
Search Results
2. EFFECTS OF pH AND TEMPERATURE ON VOLATILE CONSTITUENTS OF CARAWAY.
- Author
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YIN, YUSEN, ZARGHAMI, N., and HEINZ, D. E.
- Published
- 1970
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3. Synthesis and characterization of N-rich fluorescent bio-dots as a reporter in the design of dual-labeled FRET probe for TaqMan PCR: A feasibility study.
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Imani M, Mohajeri N, Rastegar M, and Zarghami N
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- Feasibility Studies, DNA genetics, Coloring Agents, Fluorescent Dyes chemistry, Fluorescence Resonance Energy Transfer methods, Quantum Dots
- Abstract
DNA-based analytical techniques have provided an advantageous sensing assay in the realm of biotechnology. Bio-inspired fluorescent nanodots are a novel type of biological staining agents with excellent optical properties widely used for cellular imaging and diagnostics. In the present research, we successfully synthesized bio-dots with excellent optical properties and high-quantum yield from DNA sodium salt through the hydrothermal method. We conjugated the bio-dots with 3' Eclipse Dark Quencher (Eclipse)-labeled single-strand oligodeoxyribonucleotide according to carbodiimide chemistry, to design a fluorescence resonance energy transfer (FRET) probe. The results confirmed the prosperous synthesis and surface functionalization of the bio-dot. Analysis of size, zeta potential, and FTIR spectroscopy verified successful bioconjugation of the bio-dots with probes. UV-visibility analysis and fluorescence intensity profile of the bio-dot and bio-dot@probes represented a concentration-dependent quenching of fluorescent signal of bio-dot by Eclipse after probe conjugation. The results demonstrated that TaqMan PCR was not feasible using the designed bio-dot@probes. Our results indicated that bio-dot can be used as an efficient fluorescent tag in the design of fluorescently labeled oligonucleotides with high biocompatibility and optical features., (© 2022 International Union of Biochemistry and Molecular Biology, Inc.)
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- 2023
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4. The effect of exogenous ciliary neurotrophic factor on cell cycle and neural differentiation markers of in vitro model cells: New insights for future therapeutic approaches.
- Author
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Ghasemi M, Alizadeh E, Motlagh BF, and Zarghami N
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- Cell Cycle drug effects, Cell Differentiation drug effects, Cell Proliferation drug effects, Cell Survival drug effects, Ciliary Neurotrophic Factor administration & dosage, Dietary Supplements, Dose-Response Relationship, Drug, Humans, Retinoblastoma metabolism, Retinoblastoma pathology, Tumor Cells, Cultured, Ciliary Neurotrophic Factor pharmacology, Models, Biological, Neurons drug effects, Retinoblastoma drug therapy
- Abstract
Retinoblastoma is known as childhood rare malignancy of the retina. Ciliary neurotrophic factor (CNTF) was previously found to reduce degeneration and promote retina survival. This work investigated the effects of CNTF supplementation on in-vitro model cells including retinoblastoma (Y79) and adipose-derived mesenchymal stem cells (AMSCs) viability, proliferation, gene expression and cell cycle. A drop of viability was detected in Y79 treated with CNTF in a dose-dependent manner (P < .05). However, the proliferation of AMSCs was increased at lower concentrations of CNTF (5 ng/mL), but declined in higher doses (50 and 100 ng/mL). The BrdU assay confirmed the MTT assay results. Cell cycle was arrested in both Y79 and AMSCs in the G0/G1 phase by CNTF treatment. A considerable down-regulation of Bcl2, CycD1 and N-Myc genes expression (P < .05) inversely, P15 and P21 genes up-regulation in treated Y79 cells was observed. Besides, stemness genes' transcription was reduced in AMSCs (P < .05), and levels of neuronal-specific markers such as neuron-specific enolase (NSE) and neuronal nuclei (NeuN) were increased (P < .05). The findings of this study suggest a promising potential of CNTF in terms of arresting Y79 retinoblastoma cells, and differentiation-inducing to AMSCs, which could be valuable for managing future innovative treatments targeting retinoblastoma. SIGNIFICANCE OF THE STUDY: We demonstrate that CNTF has the potential to reduce proliferation of Y79 cells and induce the cell cycle arrest of them. Also, down-regulation of oncogenes (such as N-Myc) while up-regulation of tumour suppressor genes (such as P21) was detected by exposure of Y79 cells to CNTF. Furthermore, we observed the cell cycle arrest, reduction of stemness gene and up-regulation of neural differentiation markers in AMSCs treated with CNTF. These results support the probable promising effects of CNTF for controlling retinoblastoma., (© 2021 John Wiley & Sons Ltd.)
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- 2021
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5. Spotlight on 17-AAG as an Hsp90 inhibitor for molecular targeted cancer treatment.
- Author
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Talaei S, Mellatyar H, Asadi A, Akbarzadeh A, Sheervalilou R, and Zarghami N
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- Antineoplastic Agents chemistry, Antineoplastic Agents metabolism, Antineoplastic Agents therapeutic use, Benzoquinones metabolism, Benzoquinones therapeutic use, Clinical Trials as Topic, Drug Carriers chemistry, Drug Evaluation, Preclinical, HSP90 Heat-Shock Proteins metabolism, Humans, Lactams, Macrocyclic metabolism, Lactams, Macrocyclic therapeutic use, Liposomes chemistry, Nanoparticles chemistry, Neoplasms drug therapy, Benzoquinones chemistry, HSP90 Heat-Shock Proteins antagonists & inhibitors, Lactams, Macrocyclic chemistry
- Abstract
Hsp90 is a ubiquitous chaperone with important roles in the organization and maturation of client proteins that are involved in the progression and survival of cancer cells. Multiple oncogenic pathways can be affected by inhibition of Hsp90 function through degradation of its client proteins. That makes Hsp90 a therapeutic target for cancer treatment. 17-allylamino-17-demethoxy-geldanamycin (17-AAG) is a potent Hsp90 inhibitor that binds to Hsp90 and inhibits its chaperoning function, which results in the degradation of Hsp90's client proteins. There have been several preclinical studies of 17-AAG as a single agent or in combination with other anticancer agents for a wide range of human cancers. Data from various phases of clinical trials show that 17-AAG can be given safely at biologically active dosages with mild toxicity. Even though 17-AAG has suitable pharmacological potency, its low water solubility and high hepatotoxicity could significantly restrict its clinical use. Nanomaterials-based drug delivery carriers may overcome these drawbacks. In this paper, we review preclinical and clinical research on 17-AAG as a single agent and in combination with other anticancer agents. In addition, we highlight the potential of using nanocarriers and nanocombination therapy to improve therapeutic effects of 17-AAG., (© 2019 John Wiley & Sons A/S.)
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- 2019
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6. An integrated analysis to predict micro-RNAs targeting both stemness and metastasis in breast cancer stem cells.
- Author
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Rahimi M, Sharifi-Zarchi A, Firouzi J, Azimi M, Zarghami N, Alizadeh E, and Ebrahimi M
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- Breast Neoplasms pathology, Cell Movement genetics, Cell Proliferation genetics, Epithelial-Mesenchymal Transition genetics, Female, Gene Expression Regulation, Neoplastic genetics, Humans, Kruppel-Like Factor 4, MCF-7 Cells, MicroRNAs classification, Neoplasm Metastasis, Neoplasm Proteins classification, Neoplastic Stem Cells pathology, Breast Neoplasms genetics, MicroRNAs genetics, Neoplasm Proteins genetics, Neoplastic Stem Cells metabolism
- Abstract
Several evidences support the idea that a small population of tumour cells representing self-renewal potential are involved in initiation, maintenance, metastasis, and outcomes of cancer therapy. Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary for the identification of new targets for cancer therapy. The aim of the present study was to predict the miRNAs pattern, which can target both metastasis and self-renewal pathways using integration of literature and data mining. For this purpose, mammospheres derived from MCF-7, MDA-MB231, and MDA-MB468 were used as breast CSCs model. They had higher migration, invasion, and colony formation potential, with increasing in stemness- and EMT-related genes expression. Our results determined that miR-204, -200c, -34a, and -10b contemporarily could target both self-renewal and EMT pathways. This core regulatory of miRNAs could increase the survival rate of breast invasive carcinoma via up-regulation of OCT4, SOX2, KLF4, c-MYC, NOTCH1, SNAI1, ZEB1, and CDH2 and down-regulation of CDH1. The majority of those target genes were involved in the regulation of pluripotency, MAPK, WNT, Hedgehog, p53, and transforming growth factor β pathways. Hence, this study provides novel insights for targeting core regulatory of miRNAs in breast CSCs to target both self-renewal and metastasis potential and eradication of breast cancer., (© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)
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- 2019
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7. An overview on Vadimezan (DMXAA): The vascular disrupting agent.
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Daei Farshchi Adli A, Jahanban-Esfahlan R, Seidi K, Samandari-Rad S, and Zarghami N
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- Antineoplastic Agents pharmacology, Antineoplastic Agents therapeutic use, Clinical Trials as Topic, Cytokines metabolism, Humans, Immunity, Innate drug effects, NF-kappa B metabolism, Neoplasms drug therapy, Neoplasms pathology, Nitric Oxide metabolism, Xanthones pharmacology, Xanthones therapeutic use, p38 Mitogen-Activated Protein Kinases metabolism, Antineoplastic Agents metabolism, Xanthones metabolism
- Abstract
Vascular disrupting agents (VDAs), a group of cancer remedies, can cause a specific and irreversible destruction of established tumor vessels, and the complete halt of blood flow in the tumor. DMXAA (ASA404) or Vadimezan, a flavone-acetic acid-based drug, is the most promising VDAs that induces a rapid shutdown of blood flow in tumors but not in normal tissue. The exact mechanism of vascular disruption is unknown; however, proposed direct and indirect mechanisms of action for DMXAA comprises (i) inducing apoptosis in endothelial cells; (ii) hemorrhagic necrosis and ischemia in tumor; (iii) release of serotonin (5-HT); (vi) stimulation of innate immune system; (v) production of inflammatory cytokines, for example TNF, IL-6, GCSF, KC, IP-10, and MCP-1; (vi) activation of NFκB and p38 (MAPK); (vii) production of nitric oxide; and (viii) reducing tumor energetics and membrane turnover. Despite the remarkable results from preclinical and phase I/II, DMXAA has failed in phase III clinical trials. The reason for this surprising discrepancy, among others, was discovered to be STING receptor variations between mice and humans. In this review, the development, the mechanisms of DMXAA action, the clinical trials, the combination therapy, and the future of this drug will be discussed., (© 2017 John Wiley & Sons A/S.)
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- 2018
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8. Metformin enhances doxorubicin sensitivity via inhibition of doxorubicin efflux in P-gp-overexpressing MCF-7 cells.
- Author
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Shafiei-Irannejad V, Samadi N, Yousefi B, Salehi R, Velaei K, and Zarghami N
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- Adenosine Triphosphate metabolism, Cell Survival drug effects, Doxorubicin chemistry, Drug Resistance, Neoplasm drug effects, Flow Cytometry, Humans, MCF-7 Cells, Metformin chemistry, Rhodamine 123 chemistry, ATP Binding Cassette Transporter, Subfamily B, Member 1 metabolism, Apoptosis drug effects, Doxorubicin pharmacology, Metformin pharmacology
- Abstract
Resistance against chemotherapy is still a major problem in successful cancer treatment in the clinic. Therefore, identifying new compounds with lower side-effects and higher efficacy is an important approach to overcome multidrug resistance (MDR). Here, we investigated the activity and possible mechanism of the antidiabetic drug, metformin, in human doxorubicin (DOX)-resistant breast cancer (MCF-7/DOX) cells. The effect of metformin on the cytotoxicity of DOX was evaluated by MTT assay. The P-gp mRNA/protein expression levels following treatment with metformin were determined using real-time polymerase chain reaction and Western blot analysis, respectively. Intracellular rhodamine 123 accumulation assay was performed to evaluate the P-gp function. Cellular ATP content was determined using ATP assay kit. The effect of metformin on DOX-induced apoptosis was evaluated by annexin V/FITC assay. Exposure to metformin considerably enhanced the cytotoxicity of DOX. Metformin had no substantial effect on P-gp expression, while the activity of P-gp and intracellular ATP content decreased with metformin treatment in a dose-dependent manner. Furthermore, metformin significantly increased the DOX-induced apoptosis. These results indicate that metformin could reverse MDR in breast cancer cells by reducing P-gp activity. Therefore, metformin can be suggested as a potent adjuvant in breast cancer chemotherapy., (© 2017 John Wiley & Sons A/S.)
- Published
- 2018
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9. New insights into antidiabetic drugs: Possible applications in cancer treatment.
- Author
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Shafiei-Irannejad V, Samadi N, Salehi R, Yousefi B, and Zarghami N
- Subjects
- AMP-Activated Protein Kinase Kinases, Biguanides pharmacology, Biguanides therapeutic use, Cell Proliferation drug effects, Diabetes Mellitus, Type 2 drug therapy, Humans, Hypoglycemic Agents pharmacology, Metformin therapeutic use, Neoplasms pathology, Protein Serine-Threonine Kinases metabolism, Sulfonylurea Compounds therapeutic use, Thiazolidinediones pharmacology, Thiazolidinediones therapeutic use, Hypoglycemic Agents therapeutic use, Neoplasms drug therapy
- Abstract
Globally at 2014, it was estimated that there was 347 million people with diabetes in which 90 percent of them were diagnosed with type 2 diabetes mellitus (T2DM). Although the association between diabetes mellitus and cancer risk was found about 100 years ago, the issue is not still clear. Many studies especially cohort and case-control studies have suggested a higher risk of cancer in patients with diabetes mainly in those with type 2 diabetes. Insulin concentration is high in these patients, and due to its mitogenic effects, it may be a possible hypotheses for higher risk of cancer in diabetic patients. Therefore, antidiabetic drugs, which are involved in insulin secretion and sensitivity, may have beneficial effects in cancer treatment. Several groups of drugs with different mechanisms of action, mostly prescribed orally, are used for the treatment of type 2 diabetes mellitus including, insulin sensitizers (thiazolidinediones), insulin secretagogues (sulfonylureas), and biguanides. In this review, the possible effects of antidiabetic drugs (biguanides, thiazolidinediones, and sulfonylureas) and some of their mechanisms for overcoming cancer will be discussed., (© 2017 John Wiley & Sons A/S.)
- Published
- 2017
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10. Peroxisome Proliferator-Activated Receptor Ligands and Their Role in Chronic Myeloid Leukemia: Therapeutic Strategies.
- Author
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Yousefi B, Samadi N, Baradaran B, Shafiei-Irannejad V, and Zarghami N
- Subjects
- Animals, Apoptosis drug effects, Cation Transport Proteins metabolism, Drug Synergism, Fusion Proteins, bcr-abl metabolism, Humans, Imatinib Mesylate agonists, Imatinib Mesylate therapeutic use, Leukemia, Myelogenous, Chronic, BCR-ABL Positive metabolism, Ligands, Peroxisome Proliferator-Activated Receptors metabolism, Antineoplastic Agents therapeutic use, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Peroxisome Proliferator-Activated Receptors antagonists & inhibitors
- Abstract
Imatinib therapy remains the gold standard for treatment of chronic myeloid leukemia; however, the acquired resistance to this therapeutic agent in patients has urged the scientists to devise modalities for overcoming this chemoresistance. For this purpose, initially therapeutic agents with higher tyrosine kinase activity were introduced, which had the potential for inhibiting even mutant forms of Bcr-Abl. Furthermore, coupling imatinib with peroxisome proliferator-activated receptor ligands also showed beneficial effects in chronic myeloid leukemia cell proliferation. These combination protocols inhibited cell growth and induced apoptosis as well as differentiation in chronic myeloid leukemia cell lines. In addition, peroxisome proliferator-activated receptors ligands increased imatinib uptake by upregulating the expression of human organic cation transporter 1. Taken together, peroxisome proliferator-activated receptors ligands are currently being considered as novel promising therapeutic candidates for chronic myeloid leukemia treatment, because they can synergistically enhance the efficacy of imatinib. In this article, we reviewed the potential of peroxisome proliferator-activated receptors ligands for use in chronic myeloid leukemia treatment. The mechanism of action of these therapeutics modalities are also presented in detail., (© 2016 John Wiley & Sons A/S.)
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- 2016
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11. Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells.
- Author
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Alizadeh E, Eslaminejad MB, Akbarzadeh A, Sadeghi Z, Abasi M, Herizchi R, and Zarghami N
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- Cell Differentiation drug effects, Cell Lineage, Cells, Cultured, Down-Regulation drug effects, Hepatocyte Nuclear Factor 4 metabolism, Hepatocyte Nuclear Factor 6 metabolism, Hepatocytes cytology, Hepatocytes metabolism, Humans, alpha-Fetoproteins metabolism, Hepatocytes drug effects, Hydroxamic Acids pharmacology, Mesenchymal Stem Cells cytology, MicroRNAs metabolism, Up-Regulation drug effects
- Abstract
The miR-122 is a tissue-specific miRNA; its expression is abundant in liver. MiR-122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported previously. The aim of this study was to determine whether TSA can affect the expression of miR-122 in hepatocyte-like cells (HLCs) generated from human adipose tissue-derived mesenchymal stem cells (hAT-MSCs). The hepatic differentiation of hAT-MSCs induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLCs generated with or without TSA and the expression levels of miR-122 were studied. The expression levels of miR-122 in TSA-treated HLCs was significantly (p < 0.05) higher than those generated by growth factors and cytokines, only. The downregulation of a-fetoprotein (AFP) levels but enhanced albumin synthesis (p < 0.05) and upregulation of liver-enriched transcription factors (LETFs) HNF4α (hepatocyte nuclear factor 4α) and HNF6 (hepatocyte nuclear factor 6) were observed in TSA-treated HLCs (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT-MSCs resulted in higher expression levels of miR-122, facilitation of differentiation, and subsequently attenuation of AFP levels., (© 2015 John Wiley & Sons A/S.)
- Published
- 2016
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12. A Novel Protocol to Differentiate Induced Pluripotent Stem Cells by Neuronal microRNAs to Provide a Suitable Cellular Model.
- Author
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Zare M, Soleimani M, Akbarzadeh A, Bakhshandeh B, Aghaee-Bakhtiari SH, and Zarghami N
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- Cell Differentiation genetics, Drug Evaluation, Preclinical methods, Humans, Induced Pluripotent Stem Cells cytology, MicroRNAs biosynthesis, MicroRNAs genetics, Neural Stem Cells cytology, Neurodegenerative Diseases drug therapy, Neurons cytology, Plasmids administration & dosage, Plasmids genetics, Transduction, Genetic methods, Induced Pluripotent Stem Cells physiology, MicroRNAs administration & dosage, Neural Stem Cells physiology, Neurodegenerative Diseases genetics, Neurodegenerative Diseases pathology, Neurons physiology
- Abstract
Neurodegenerative diseases are one of the most challenging subjects in medicine. Investigation of their underlying genetic or epigenetic factors is hampered by lack of suitable models. Patient-specific induced pluripotent stem cells (iPS cells) represent a valuable approach to provide a proper model for poorly understood mechanisms of neuronal diseases and the related drug screenings. miR-124 and miR-128 are the two brain-enriched miRNAs with different time-points of expression during neuronal development. Herein, we transduced human iPS cells with miR-124 and miR-128 harboring lentiviruses sequentially. The transduced plasmids contained GFP and puromycin antibiotic-resistant genes for easier selection and identification. Morphological assessment and immunocytochemistry (overexpressions of beta-tubulin and neuron-specific enolase) confirmed that induced hiPS cells by miR-124 and miR-128 represent similar characteristics to those of mature neurons. In addition, the upregulation of neuron-specific enolase, beta-tubulin, Map2, GFAP, and BDNF was detected by quantitative real-time PCR. In conclusion, it seems that our novel protocol remarks the combinatorial effect of miR-124 and miR-128 on neural differentiation in the absence of any extrinsic factor. Moreover, such cellular models could be used in personalized drug screening and applied for more effective therapies., (© 2014 John Wiley & Sons A/S.)
- Published
- 2015
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13. Up regulation of liver-enriched transcription factors HNF4a and HNF6 and liver-specific microRNA (miR-122) by inhibition of let-7b in mesenchymal stem cells.
- Author
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Alizadeh E, Akbarzadeh A, Eslaminejad MB, Barzegar A, Hashemzadeh S, Nejati-Koshki K, and Zarghami N
- Subjects
- Adipose Tissue cytology, Adult, Cell Differentiation, Cell Survival, Cells, Cultured, Female, G1 Phase Cell Cycle Checkpoints, Hep G2 Cells, Hepatocyte Nuclear Factor 4 metabolism, Hepatocyte Nuclear Factor 6 metabolism, Hepatocytes cytology, Hepatocytes metabolism, Humans, Male, Mesenchymal Stem Cells cytology, Middle Aged, Oligonucleotides, Antisense genetics, Oligonucleotides, Antisense metabolism, Hepatocyte Nuclear Factor 4 genetics, Hepatocyte Nuclear Factor 6 genetics, Liver metabolism, Mesenchymal Stem Cells metabolism, MicroRNAs genetics, MicroRNAs metabolism, Up-Regulation
- Abstract
MicroRNAs are small non-coding RNAs that regulate key processes of the stem cells. Although, microRNAs have emerged as powerful regulators of differentiation, few studies have been focused on the post-transcriptional regulation of hepatic differentiation in mesenchymal stem cells (MSCs) by microRNAs. The aim of this study was to evaluate the specific effect of let-7 microRNAs in particular let-7b in hepatic commitment of human adipose tissue-derived mesenchymal stem cells (hAT-MSCs). The dynamic expression profile of let-7a, b, c microRNAs and two liver-enriched transcription factors (LETFs) HNF4a and HNF6 was studied during in vitro hepatic differentiation of hAT-MSCs. Let-7b was used for transient overexpression and knockdown investigations. It was shown that the expression of LETFs is inversely correlated with those of let-7 miRNAs during differentiation progress (p < 0.05). Inhibition of let-7b caused upregulation of LETFs, an increase in the expression of miR-122 (p < 0.01) emulating the features of functional hepatocytes, and accumulation of hAT-MSCs in the G0 /G1 phase of cell cycle, triggering initiation of hepatic commitment. In conclusion, transient inhibition of let-7b activates hepatic differentiation of hAT-MSCs. The findings of this work might help optimization of in vitro hepatogenic differentiation utilizing microRNAs and hAT-MSCs that could be used for therapeutic purposes., (© 2014 John Wiley & Sons A/S.)
- Published
- 2015
- Full Text
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