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Berlin Brandenburg

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  • 1
    Language: English
    In: Molecular Medicine Reports, 12/2015, Vol.12(6), pp.8282-8288
    Description: Cardiomyocyte hypertrophy is a threat to human health due to the probability of sudden heart failure-induced mortality. Previous studies have demonstrated that nuclear factor of activated T cells cytoplasmic 3 (NFATC3) is important in the process of cardiomyocyte hypertrophy. However, the molecular mechanism underlying the alteration in the expression levels of NFATC3 during cardiomyocyte hypertrophy has remained to be fully elucidated. In order to shed light on the molecular mechanism, the present study employed several approaches, including the measurement of the cell surface area, analysis of the protein/DNA ratio, western blot analysis and a Luciferase reporter assay using isolated rat cardiomyocytes as model. The results showed that expression of microRNA-1 ( miR-1 ) was reduced in patients diagnosed with cardiac hypertrophy and rat cardiomyocytes treated with pro-hypertrophic stimuli. The increase in the expression of miR-1 was able to inhibit the hypertrophic remodeling of cardiomyocytes. The suppression of miR-1 was sufficient to induce cardiomyocyte hypertrophy, and further experiments confirmed that NFATC3 was a target of miR-1 in cardiomyocytes. Forced expression of NFATC3 inhibited the protective activity of miR-1 against hypertrophic stimuli in the cardiomyocytes. These findings provided clarification of the regulatory signaling pathway underlying cardiac hypertrophy, and provided evidence that targeting the miR-1 /NFATC3 pathway may be a promising strategy for the prevention and treatment of heart hypertrophy.
    Keywords: Microrna-1 ; Nuclear Factor Of Activated T Cells Cytoplasmic 3 ; Cardiomyocyte ; Hypertrophy
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 2
    Language: English
    In: Molecular Medicine Reports, 2014, Vol.9(5), p.1834(5)
    Description: The inflammatory response has adverse effects on left ventricular (LV) function and remodeling post-myocardial infarction (MI). Interleukin (IL)-33 is considered to have anti-inflammatory properties. The present study examined whether the suppression of inflammation with IL-33 was able to attenuate LV dysfunction and remodeling post-MI. The MI model was induced and the mice were treated with either saline or recombinant IL-33. Inflammatory mediators, LV functional changes and structural remodeling were evaluated. IL-33 significantly suppressed macrophage infiltration and the production of inflammatory cytokines in the myocardium. IL-33 treatment significantly improved LV function, reduced infarct size and infarct wall thinning. MI-induced activation of the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-[kappa]B (NF-[kappa]B) pathways was also suppressed. Our data demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-[kappa]B pathways. IL-33 may be a potential therapeutic target for heart dysfunction post-MI. Key words: IL-33, myocardial infarction, inflammation, cardiac remodeling
    Keywords: Interleukins – Health Aspects ; Heart Attack – Health Aspects ; Anti-Inflammatory Agents – Health Aspects ; Inflammation – Health Aspects
    ISSN: 1791-2997
    E-ISSN: 17913004
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Molecular Medicine Reports, 7/2015, Vol.12(1), pp.1002-1008
    Description: Somatostatin (SST) is a neuromodulator which is abundant throughout the central nervous system (CNS) and has a crucial role in neurodegenerative disorders. However, little is known about the effects and mechanisms of SST in dopaminergic (DA) neurons in the context of Parkinson’s disease (PD). In the present study, a model of PD was generated by injecting lipopolysaccharide (LPS) into the substantia nigra (SN) of rats in order to investigate the effects of SST on LPS-induced degeneration of DA in vivo . Intramural injection of LPS resulted in a significant loss of DA neurons, while reduction of neuronal death by SST pretreatment was confirmed using immunohistochemical staining for tyrosine hydroxylase and Nissl. In parallel, immunohistochemical detection of OX-42 and hydroethidine staining were employed to determine the activation of microglia and production of reactive oxygen species (ROS), respectively. It was found that SST inhibited the LPS-induced microglial activity and ROS production. ELISA revealed a decreased production of pro-inflammatory mediators, including tumor necrosis factor-α, interleukin-1β and prostaglandin E2 when SST was administered prior to LPS treatment. Western blot analysis showed that LPS-induced expression of inducible nitric oxide synthase, cyclooxygenase-2 and nuclear factor κB (NF-κB) p-p65 was attenuated by administration of SST prior to LPS application. The results indicated that LPS-induced loss of nigral DA neurons was inhibited by SST and the observed effects of SST on neuroprotection were associated with suppression of microglial activation and the NF-κB pathway, ensuing decreases of neuroinflammation and oxidative stress. The present study therefore suggested that SST is beneficial for treating neurodegenerative diseases, such as PD, through inhibiting the activation of microglia.
    Keywords: Somatostatin ; Neuron ; Substantia Nigra ; Microglia ; Parkinson’s Disease
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 4
    Language: English
    In: Molecular Medicine Reports, 11/2015, Vol.12(5), pp.6568-6576
    Description: Schizophrenia (SCZ) is one of the most complex mental illnesses affecting ~1% of the population worldwide. SCZ pathogenesis is considered to be a result of genetic as well as epigenetic alterations. Previous studies have aimed to identify the causative genes of SCZ. However, DNA methylation of long non-coding RNAs (lncRNAs) involved in SCZ has not been fully elucidated. In the present study, a comprehensive genome-wide analysis of DNA methylation was conducted using samples from two male patients with paranoid and undifferentiated SCZ, respectively. Methyl-CpG binding domain protein-enriched genome sequencing was used. In the two patients with paranoid and undifferentiated SCZ, 1,397 and 1,437 peaks were identified, respectively. Bioinformatic analysis demonstrated that peaks were enriched in protein-coding genes, which exhibited nervous system and brain functions. A number of these peaks in gene promoter regions may affect gene expression and, therefore, influence SCZ-associated pathways. Furthermore, 7 and 20 lncRNAs, respectively, in the Refseq database were hypermethylated. According to the lncRNA dataset in the NONCODE database, ~30% of intergenic peaks overlapped with novel lncRNA loci. The results of the present study demonstrated that aberrant hypermethylation of lncRNA genes may be an important epigenetic factor associated with SCZ. However, further studies using larger sample sizes are required.
    Keywords: Schizophrenia ; Dna Methylation ; Protein Coding Gene ; Long Non-Coding Rna
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 5
    Language: English
    In: Molecular Medicine Reports, May, 2014, Vol.9(5), p.1834(5)
    Description: The inflammatory response has adverse effects on left ventricular (LV) function and remodeling post-myocardial infarction (MI). Interleukin (IL)-33 is considered to have anti-inflammatory properties. The present study examined whether the suppression of inflammation with IL-33 was able to attenuate LV dysfunction and remodeling post-MI. The MI model was induced and the mice were treated with either saline or recombinant IL-33. Inflammatory mediators, LV functional changes and structural remodeling were evaluated. IL-33 significantly suppressed macrophage infiltration and the production of inflammatory cytokines in the myocardium. IL-33 treatment significantly improved LV function, reduced infarct size and infarct wall thinning. MI-induced activation of the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-[kappa]B (NF-[kappa]B) pathways was also suppressed. Our data demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-[kappa]B pathways. IL-33 may be a potential therapeutic target for heart dysfunction post-MI. Key words: IL-33, myocardial infarction, inflammation, cardiac remodeling
    Keywords: Interleukins -- Health Aspects ; Left Heart Ventricle -- Abnormalities ; Heart Attack -- Complications And Side Effects ; Molecular Targeted Therapy -- Innovations
    ISSN: 1791-2997
    ISSN: 17913004
    E-ISSN: 17913004
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  • 6
    Language: English
    In: Molecular Medicine Reports, 09/2016, Vol.14(3), pp.2732-2738
    Description: Aberrant promoter methylation of multiple genes is associated with various diseases, including Alzheimer's disease (AD). The goal of the present study was to determine whether dopamine receptor D4 (DRD4) promoter methylation is associated with AD. In the current study, the methylation levels of the DRD4 promoter were measured in 46 AD patients and 61 controls using bisulfite pyrosequencing technology. The results of the present study demonstrated that DRD4 promoter methylation was significantly higher in AD patients than in controls. A further breakdown analysis by gender revealed that there was a significant association of DRD4 promoter methylation with AD in males (23 patients and 45 controls). In conclusion, the results of the present study demonstrated that elevated DRD4 promoter methylation was associated with AD risk in males.
    Keywords: Alzheimer'S Disease ; Dopamine Receptor D4 ; Dna Methylation ; Promoter ; Male ; Epigenetics
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 7
    Language: English
    In: Molecular Medicine Reports, 01/2018, Vol.17(1), pp.1015-1021
    Description: Severe aplastic anemia (SAA) is a primary disorder of severe bone marrow failure characterizing with extreme pancytopenia and a profound diminution of bone marrow progenitor cells, which is associated with T cell hyper-function. Abnormal telomere shortening of bone marrow mononuclear cell has been reported in AA, which may lead to genomic instability, and result in cell senescence or apoptosis. Notably, certain studies identfieid that lymphocytes of shortening telomere length have undergone apoptosis escape in autoimmune diseases. In order to investigate the association between telomere lengths and function of T lymphocytes in SAA, the relative telomere lengths (RTLs) of different subtypes of T lymphocytes were investigated by flow-fluorescent in situ hybridization in 30 patients with SAA and 25 healthy controls. Then the levels of expression of cluster of differentiation 28 (CD28), CD158 and CD70 were measured, which represent the function of T lymphocytes. The apoptosis rate and the cell cycle progression of CD8 + T lymphocytes, and the level of secretion interferon-γ and tumor necrosis factor-α were also measured. Finally, the correlation between telomere length and these functional events of CD8 + T lymphocytes was analyzed in patients with SAA. The results showed that RTLs of CD8 + T lymphocytes in SAA were significantly shorter compared with those in controls. Furthermore, in patients with SAA, CD8 + T lymphocytes are associated with T cell hyper-function, which is related to the RTL. Thus, the shorter RTLs of CD8 + T lymphocytes in SAA may be associated with hyper-function of these cells, which contribute to the pathogenesis of SAA.
    Keywords: Severe Aplastic Anemia ; Telomere Length ; T Lymphocytes ; Cd28 ; Cd158 ; Cd70
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 8
    Language: English
    In: Molecular Medicine Reports, 9/2014, Vol.10(3), pp.1252-1258
    Description: The aim of the present study was to investigate the number and function of CD8 + HLA-DR + cells, which are considered to be activated cytotoxic T lymphocytes (CTLs), in peripheral blood to further examine the pathogenesis of severe aplastic anemia (SAA). Thirty-eight patients with SAA were included in the present study. Patients were screened for paroxysmal nocturnal hemoglobinuria by flow cytometry using anti-CD55 and anti-CD59 antibodies. The number of CD8 + HLA-DR + T cells was measured by three-color flow cytometry using anti-CD8-peridinin chlorophyll, anti-CD3-fluorescein isothiocyanate (FITC) and anti-HLA-DR-FITC antibodies. The expression of perforin, granzyme B, tumor necrosis factor-β (TNF-β) and FasL in CD8 + HLA-DR + T cells was detected by flow cytometry with the appropriate monoclonal antibodies. Total RNA was prepared from purified CD8 + HLA-DR + cells of healthy controls and SAA patients, and then polymerase chain reaction (PCR) was performed. Apoptosis of CD8 + HLA-DR + cells was detected by flow cytometry following staining with Annexin V. The proportion of CD8 + HLA-DR + T cells was analyzed by flow cytometry in peripheral blood and was identified to be significantly higher in untreated SAA than in remission patients and in the controls. The expression of perforin, granzyme B, TNF-β and FasL in CD8 + HLA-DR + T cells was analyzed by flow cytometry and PCR, which revealed increased expression in the untreated SAA group compared with that in the control group. Furthermore, the apoptosis of CD3 − bone marrow cells from normal individuals was enhanced following co-culture with CD8 + HLA-DR + T cells from untreated SAA patients. In conclusion, the present study demonstrated that CD8 + HLA-DR + T cells may contribute to bone marrow failure in SAA.
    Keywords: Anemia ; Aplastic ; Cd8hla-Dr T Cells ; Apoptosis
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 9
    Language: English
    In: Molecular Medicine Reports, Sept, 2014, Vol.10(3), p.1252(7)
    Description: The aim of the present study was to investigate the number and function of [CD8.sup.+]HLA-[DR.sup.+] cells, which are considered to be activated cytotoxic T lymphocytes (CTLs), in peripheral blood to further examine the pathogenesis of severe aplastic anemia (SAA). Thirty-eight patients with SAA were included in the present study. Patients were screened for paroxysmal nocturnal hemoglobinuria by flow cytometry using anti-CD55 and anti-CD59 antibodies. The number of [CD8.sup.+]HLA-[DR.sup.+] T cells was measured by three-color flow cytometry using anti-CD8-peridinin chlorophyll, anti-CD3-fluorescein isothiocyanate (FITC) and anti-HLA-DR-FITC antibodies. The expression of perforin, granzyme B, tumor necrosis factor-[beta] (TNF-[beta]) and FasL in [CD8.sup.+]HLA-[DR.sup.+] T cells was detected by flow cytometry with the appropriate monoclonal antibodies. Total RNA was prepared from purified [CD8.sup.+]HLA-[DR.sup.+] cells of healthy controls and SAA patients, and then polymerase chain reaction (PCR) was performed. Apoptosis of [CD8.sup.+]HLA-[DR.sup.+] cells was detected by flow cytometry following staining with Annexin V. The proportion of [CD8.sup.+]HLA-[DR.sup.+] T cells was analyzed by flow cytometry in peripheral blood and was identified to be significantly higher in untreated SAA than in remission patients and in the controls. The expression of perforin, granzyme B, TNF-[beta] and FasL in [CD8.sup.+]HLA-[DR.sup.+] T cells was analyzed by flow cytometry and PCR, which revealed increased expression in the untreated SAA group compared with that in the control group. Furthermore, the apoptosis of [CD3.sup.-] bone marrow cells from normal individuals was enhanced following co-culture with [CD8.sup.+]HLA-[DR.sup.+] T cells from untreated SAA patients. In conclusion, the present study demonstrated that [CD8.sup.+]HLA-[DR.sup.+] T cells may contribute to bone marrow failure in SAA. Key words: anemia, aplastic, [CD8.sup.+]HLA-[DR.sup.+] T cells, apoptosis
    Keywords: Aplastic Anemia -- Genetic Aspects ; Aplastic Anemia -- Development And Progression ; Cd8 Lymphocytes -- Identification And Classification
    ISSN: 1791-2997
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