Molecular Medicine Reports (Mol Med Rep )

Description

  • Impact factor
    1.17
  • 5-year impact
    0.96
  • Cited half-life
    1.90
  • Immediacy index
    0.26
  • Eigenfactor
    0.00
  • Article influence
    0.22
  • Website
    Molecular Medicine Reports website
  • ISSN
    1791-2997
  • OCLC
    248467032
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Inflammatory response and cardiomyocyte apoptosis are important processes in ventricular remodeling post‑myocardial infarction (MI) and may form the basic mechanisms in the development of chronic heart failure. The nuclear factor κB (NF‑κB) signaling pathway could promote inflammation and apoptosis and it has been demonstrated that lycopene inhibits cigarette smoke extract‑mediated NF‑κB activation. Therefore, it was hypothesized that the NF‑κB signaling pathway may be a key target of lycopene in the reversal of ventricular remodeling post MI. An MI model was established by left anterior descending coronary artery ligation in mice. Following ligation, the mice were administered with lycopene (10 mg/kg/day) or saline. The mice underwent echocardiography and were sacrificed after 4 weeks. The mRNA expression of fibrosis markers transforming growth factor‑β1 (TGF‑β1), collagen I and III and inflammatory markers tumor necrosis factor‑α (TNF‑α) and interleukin‑1β (IL‑1β) were examined by quantitative polymerase chain reaction. The protein expression of apoptotic markers, including caspase‑3, ‑8, ‑9 and activation of the NF‑κB signaling pathway were analyzed by western blotting. Lycopene reduced the expression of TGF‑β1, collagen I, collagen III, TNF‑α, IL‑1β, caspase‑3, ‑8 and ‑9 and inhibited the activation of the NF‑κB signaling pathway. The level of ventricular remodeling post‑MI was also attenuated following treatment with lycopene. Lycopene may inhibit the NF‑κB signaling pathway thereby reducing the inflammatory response and cardiomyocyte apoptosis post‑MI, which could be a key mechanism of lycopene in attenuating ventricular remodeling.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: The mitochondrial genome DNA copy number is critical for the functional maintenance of the mitochondria and energy acquisition for cell metabolism. Epithelial to mesenchymal transition (EMT) is an important process during embryonic development and has also been hypothesized to exhibit a significant role in cancer cell invasion and metastasis. In the present study, EMT was induced in the A549 non‑small cell lung cancer (NSCLC) cell line, using transforming growth factor‑β1 (TGF‑β1) and changes in mitochondrial content, mitochondrial DNA (mtDNA) copy number and protein cytochrome c (Cyt c) were determined by reverse transcritpion‑quantitative polymerase chain reaction and western blot analysis, respectively. mtDNA copy number and Cyt c protein levels were observed to increase following the induction of EMT in NSCLC cells. Results of the current study indicate that energy metabolism is adapted to facilitate EMT in NSCLC cells.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Vanishing lung syndrome, also known as idiopathic giant bullous emphysema, is a rare disease characterized by giant emphysematous bullae. The disease is diagnosed by radiological findings of giant bullae in one, or both, of the upper lobes of the lung, occupying at least one‑third of the hemithorax. There have been several reports of vanishing lung syndrome, however it remains to be determined whether genetic inheritance is associated with the disease. In the present study, five patients within one family, with vanishing lung syndrome, were reported during a follow‑up period of ~20 years. All of the patients were diagnosed by radiological findings, which showed diffuse bullae in the lungs, which were of varying size and asymmetrical distribution, and the occurrence of pneumothorax or emphysema. The Medical Ethics Committee of the People's Hospital of Zhangye Municipality (Zhangye, China) approved this study, and all subjects gave their informed consent During the follow‑up period of 20 years, bullae in these patients were shown to progressively increase, and no other pulmonary diseases, including lung cancer, tuberculosis, pneumoconiosis and chronic bronchitis were observed. Autosomal dominant inheritance was observed in five cases, and autosomal recessive inheritance was observed in one case. The present study suggests that vanishing lung syndrome may be associated with autosomal dominant and recessive genetic inheritance.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Plants from the Nitraria genus, members of the Zygophyllaceae family, grow naturally in Europe, Africa, Australia and the central Asian desert. Previous pharmacological research has provided evidence that members of the Nitraria genus have numerous beneficial effects. In the present review, the pharmacological and phytochemical studies of Nitraria were presented and assessed. The review was written using information published between 1968 and 2013 from a number of reliable sources, including ScienceDirect, Springer, PubMed, EMBASE and CNKI. Numerous compounds, such as alkaloids and flavonoids have been isolated from the plants of this genus in the past, and multiple members of these constituents have been demonstrated to exert antitumor or anti‑oxidative activities. The extracts of plants of the Nitraria genus possess antitumor, antiproliferative, anti‑oxidative, antifatigue, anti‑mutagenic, antimicrobial, hypotensive, hepatoprotective, lipid‑lowering and hypoglycemic effects. However, the possible active components in the fraction and the molecular mechanisms require further investigation prior to their use in clinical practice.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: microRNAs (miRNAs) have been demonstrated to play crucial roles in tumorigenesis. However, the molecular mechanism underlying the roles of miRNAs in breast cancer remains largely unknown. In this study, we showed that miR‑335 is downregulated in a number of breast cancer tissues and cell lines. Luciferase reporter assays identified the paired box 6 gene (PAX6) as a novel target of miR‑335. Further investigation revealed that miR‑335 negatively regulates the expression of PAX6 in human breast cancer MCF‑7 cells. Our results further suggested that overexpression of miR‑335 inhibits MCF‑7 cell proliferation by inducing cell‑cycle arrest at the G1 phase via targeting PAX6. Western blot analysis showed that overexpression of miR‑335 promotes p27 protein expression but inhibits cyclin D1 expression in MCF‑7 cells; however, overexpression of PAX6 decreased the p27 protein level but increased the cyclin D1 protein level in MCF‑7 cells. Furthermore, miR‑335 overexpression reduced colony formation and cellular invasion in MCF‑7 cells, an effect that was reversed by PAX6 overexpression. In conclusion, this study provides novel insights into the in vitro regulatory patterns of miRNA‑335 and PAX6 in breast cancer, and indicates that miRNA‑335 may constitute a promising candidate for the treatment of breast cancer.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Intrahepatic T helper (Th)17 cytokine and serum interleukin (IL)‑17 levels in patients with hepatitis B are positively correlated with the progression of liver cirrhosis (LC). IL‑35 can significantly inhibit the differentiation of Th17 cells and the synthesis of IL‑17. The present study aimed to investigate the function and expression of IL‑17 and IL‑35 in the blood of patients with hepatitis B‑related LC. The levels of IL‑17 and IL‑35 in the peripheral blood of 30 patients with chronic hepatitis B (CHB), 79 with LC, 14 with chronic severe hepatitis B (CSHB), and 20 normal controls were detected by ELISA. Quantitative polymerase chain reaction was used to evaluate Epstein‑Barr virus‑induced gene 3 (EBI3), forkhead box (FOX)P3 and IL‑17 mRNA expression levels in peripheral blood mononuclear cells (PBMCs). Western blotting was used to determine protein expression. The liver function of patients and normal controls was measured. EBI3, IL‑17 and FOXP3 mRNA expression levels in PBMCs from patients with LC, CHB and CSHB were higher than those in cells from the controls. IL‑17 mRNA levels differed significantly according to the Child‑Pugh classification and exhibited an upward trend over time in contrast to a downward trend for EBI3 and FOXP3 mRNA. The changes in protein expression in the peripheral blood were consistent with the changes in mRNA expression. Serum IL‑17 levels were positively correlated with total bilirubin (TBIL), alanine aminotransferase (ALT) and Child‑Pugh grade, and were negatively correlated with albumin. These observed differences were significant. Serum IL‑35 levels were negatively correlated with albumin, but not with Child‑Pugh grade, ALT and TBIL. IL‑17 and IL‑35 may be critically involved in the pathogenesis of hepatitis B‑related LC.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Cisplatin resistance is a major challenge in the clinical treatment of ovarian cancer, of which the underlying mechanisms remain unknown. The aim of the present study was to explore the role of autophagy in cisplatin resistance in ovarian cancer cells. A2780cp cisplatin‑resistant ovarian carcinoma cells and the A2780 parental cell line, were used as a model throughout the present study. The cell viability was determined using a water soluble tetrazolium salt‑8 assay, and western blot analysis was performed to determine the protein expression levels of microtubule‑associated protein 1 light chain 3 (LC3 I and LC3 II), and Beclin 1. Beclin 1 small interfering (si)RNA and 3‑methyladenine (3‑MA) were used to determine whether inhibition of autophagy may re‑sensitize cisplatin‑resistant cells to cisplatin. The ultrastructural analysis of autophagosomes was performed using transmission electron microscopy, and apoptosis was measured by flow cytometry. In both A2780cp and A2780 cells, cisplatin induced the formation of autophagosomes and upregulated the expression levels of autophagy protein markers, LC3 II and Beclin 1. However, the levels of autophagy were significantly higher in A2780cp cells, as compared with the A2780 cells. The combined treatment of cisplatin with 3‑MA, the autophagy pharmacological inhibitor, increased the cell death rate, but had no effects on apoptosis, as compared with cisplatin treatment alone in A2780cp cells. However, inhibition of autophagy by siRNA knockdown of Beclin 1 expression enhanced cisplatin‑induced cell death and apoptosis. The findings of the present study suggest that autophagy has a protective role in human ovarian cancer cells, and that targeting autophagy may promote chemotherapeutic sensitivity.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: microRNAs (miRNAs) are small, non‑coding RNAs involved in multiple biological pathways by regulating post‑transcriptional gene expression. Previously, autophagy has been reported to suppress the progression of non‑small cell lung cancer (NSCLC). However, how miRNAs regulate autophagy in NSCLC remains to be elucidated. In the present study, the autophagy gene, autophagy‑related 2B (ATG2B), was identified as a novel target of miR‑143. The overexpression of miR‑143 was able to downregulate the expression of atg2b at the transcriptional and translational levels by direct binding to its 3' untranslated region. Cell proliferation was significantly inhibited by the ectopic expression of miR‑143 in H1299 cells. Knockdown of ATG2B resulted in a similar phenotype, with the overexpression of miR‑143 in NSCLC cells. Furthermore, knockdown of ATG2B and hexokinase 2, a key enzyme in glycolysis and another target of miR‑143, co‑ordinated to inhibit the proliferation of H1299 cells. The results of the present study demonstrated that miR‑143 was a novel and important regulator of autophagy by targeting ATG2B and repression of gene expression in autophagy and high glycolysis had a coordinate effect in H1299 cells. These results suggested that ATG2B may be a new potential therapeutic target for NSCLC. Furthermore, it was implied that interrupting autophagy and glycolysis improves NSCLC therapy.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Calcium levels in the lens rise with increasing age and increased intracellular calcium accumulation is known to be a risk factor for cataract formation. Calbindin‑D28K (CALB1) is an intracellular calcium buffer. It is not clear whether CALB1 levels change in response to the Ca2+ accumulation in the lens that occurs with age. The present study investigated the distribution of CALB1 in the lenses of Sprague‑Dawley (SD) rats and whether this changed with age. Lenses were isolated from SD rats at 1, 6, 12 and 18 months of age. CALB1 distribution was examined using immunohistochemistry. Lens epithelial cells were counted in median sagittal plane slices from the hematoxylin and eosin‑stained lens and quantified using western blot analysis. Calb1 gene expression was examined using reverse transcription‑quantitative polymerase chain reaction. CALB1 was distributed in the epithelial and fiber cells of the lens. CALB1 levels declined significantly with increasing age, whilst there was no significant accompanying decrease in the number of lens cells. A similar reduction was noted in CALB1 mRNA levels. To the best of our knowledge, this is the first study to demonstrate that CALB1 expression and CALB1 protein levels in SD rat lens decrease with age. This reduction does not reflect a reduction in lens cell numbers but a genuine reduction in gene expression within these cells. Thus, CALB1 may be important in changes occurring in the lens in older age, in particular in the development of cataracts.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: The present study aimed to investigate whether gonadotropin‑releasing hormone analogues (GnRH‑as), including GnRH agonists and antagonists, affect endometrial homeobox (Hox) a10 DNA methylation during the implantation window in mice. GnRH analogue mouse models were used and were treated with either human menopausal gonadotropin (HMG) and a GnRH agonist or HMG and a GnRH antagonist. Uterus samples were collected 48 h after GnRH analogue treatment or ovulation. Bisulfite sequencing polymerase chain reaction (PCR), quantitative-PCR and western blot analysis were performed to assess Hoxa10 and integrin β3 expression. Scanning electron microscope analyses were conducted to analyze pinopode development. Compared with the natural cycle control mice, mice in the GnRH analogue groups were found to exhibit increased levels of methylation at the Hoxa10 promoter, decreased Hoxa10 mRNA and protein expression and disrupted pinopode development. These findings suggest that GnRH‑as may be associated with altered Hoxa10 DNA methylation, thus GnRH‑as may affect uterine Hoxa10 expression and endometrial receptivity.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Cisplatin is commonly used as a therapeutic agent, despite its known adverse side effects and the occurrence of drug resistance. The development of novel methods for combination therapy with cisplatin is required in order to circumvent these limitations of cisplatin alone. The proteasome inhibitor lactacystin (LAC) has been indicated to produce anti‑tumor effects, and has previously been used as an antitumor agent in cancer treatment research; however, its effects in combination with cisplatin treatment are unknown. In the current study, the effects of LAC in combination with cisplatin treatment were investigated in HeLa human cervical cancer (HCC) cells. The results demonstrated that cisplatin treatment inhibited cell growth and induced cell apoptosis. HeLa cell exposure to cisplatin induced endoplasmic reticulum (ER) stress‑associated apoptosis, and LAC treatment increased levels of cell apoptosis and the activation of caspase‑3. Specifically, LAC treatment increased the cisplatin‑induced expression of PDI, GRP78, CHOP, cleaved caspase‑4 and cleaved caspase‑3. Together, these data indicate that LAC is able to enhance cisplatin cytotoxicity by increasing ER stress‑associated apoptosis in HeLa cells.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Acute lung injury (ALI) is a common complication following intestinal ischemia/reperfusion (I/R) and is a major contributing factor to its high mortality rate. Sirtuin 1 (SIRT1), a NAD+‑dependent deacetylase, has been reported to have an important role in apoptosis inhibition, oxidative stress resistance and cell lifespan extension through its deacetylation of forkhead box protein O3 (FOXO3). It has been demonstrated that icariin (ICA), a flavonoid extracted from Epimedium, upregulates SIRT1 expression. The aim of the present study was to examine whether ICA‑mediated SIRT1/FOXO3 signaling pathway activation had a protective effect on intestinal I/R‑induced ALI. The effects of ICA on intestinal I/R‑induced ALI and its regulation of the SIRT1/FOXO3 signaling pathway on intestinal I/R‑induced ALI were investigated in rats. The results demonstrated that ICA pretreatment markedly reduced intestinal I/R‑induced ALI as indicated by histological alterations, including decreased tumor necrosis factor‑α (TNF‑α), interleukin 6 (IL‑6), reduced oxidative stress, acetylated FOXO3 and B‑cell lymphoma 2 (Bcl‑2)‑interacting mediator of cell death levels, and increased glutathione (GSH), GSH peroxidase, SIRT1, manganese superoxide dismutase and Bcl‑2 levels in rat lung tissues. Furthermore, ICA pretreatment upregulated SIRT1 expression, which then downregulated FOXO3 acetylation. In conclusion, ICA exhibited significant protective effects in intestinal I/R‑induced ALI. The protective effect of ICA may be attributed to the upregulation of SIRT1, which contributed to FOXO3 deacetylation and the modulation of downstream antioxidative and anti‑apoptotic factors.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: The identification of induced pluripotent stem cell (iPSC) technology represents great potential for recapitulating complex physiological phenotypes, probing toxicological testing and screening candidate drugs, demonstrating novel mechanistic insights and, in particular, applying iPSC-based therapeutic strategies for inherited disorders. Inherited arrhythmias are caused by various genetic abnormalities and harbor similar clinical outcomes. Clinically, the poorest outcomes are fatal arrhythmias and sudden cardiac death. However, the current therapeutic options for inherited arrhythmias are inadequate and problematic. In this review, we summarize the advances of the iPSC technique in the field of inherited arrhythmias and discuss the possibility of iPSC‑based therapies for inherited arrhythmias. Additionally, we highlight the key challenges faced in the field of iPSC and the emerging strategies used to address these concerns before the novel technique can be used safely and efficiently in clinical practice. It is likely that the iPSC technique will present opportunities and further challenges in the future.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: The aim of the current study was to observe the effects of suppressor of cytokine signaling 1 (SOCS1) silencing in human melanoma cells on cell biological behavior and interferon‑γ (IFN‑γ) sensitivity, and to investigate the use of SOCS1 as a therapeutic target in the treatment of melanoma. Western blot analysis and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) were used to verify that SOCS1 interference effectively silenced the expression of SOCS1 in the Mel526 human melanoma cell line. For IFN‑γ stimulation, western blot analysis was used to observe changes in expression levels of signal transduction and transcription activator (STAT) 1 and phosphorylated STAT (pSTAT) 1. Changes in the expression levels of IFN‑γ regulatory factor 1 (IRF‑1) were measured with RT‑qPCR. Changes in the sensitivity of melanoma cells to IFN‑γ were detected using an MTT assay. The cell proliferation rate was observed by cell counting and changes in the cell cycle were detected with flow cytometry. The results revealed that SOCS1 interference effectively silences SOCS1 expression in Mel526 cells. However, the S stage of the cell cycle was markedly extended. Following the inhibition of SOCS1 expression, the proliferation experiment demonstrated that the proliferation ability of Mel526 cells was decreased. Following IFN‑γ stimulation, the expression levels of pSTAT and IRF‑1 increased significantly compared with those in the controls. The MTT experiment showed that SOCS1 interference caused the median inhibitory concentration (IC50) of oxaliplatin in Mel526 cells to decrease significantly. In conclusion, SOCS1 interference reduced the proliferation ability of Mel526 human melanoma cells and increased their sensitivity to IFN‑γ.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Chronic hepatitis B (CHB) is one of the most common infectious disease worldwide and a leading cause of death. Hepatitis B surface antigen (HBsAg) has previously been proven to be a steady biomarker that may be used to predict clinical outcomes. The amount of circulating HBsAg has been reported to reflect the number of infected hepatocytes. An advantage of pegylated interferon alpha (peg‑IFN‑α) is that as a finite course of therapy, it can potentially lead to sustained disease remission in subsequent decades. HBsAg seroclearance can reportedly be achieved in some hepatitis B patients treated with peg‑IFN‑α; this is a major advantage of IFN‑α, as compared with nucleoside analogue treatment. In the present study, a random phage display peptide library was used to screen for potential serum peptide biomarkers in predicting which patients with CHB would exhibit HBsAg seroclearance, following 48 weeks of peg‑IFN‑α therapy. A total of 30 patients with CHB who achieved HBsAg seroclearance following peg‑IFN‑α therapy and an additional 30 age‑, gender‑, hepatitis B e antigen (HBeAg) status‑ and hepatitis B virus genotype‑matched patients with CHB without HBsAg seroclearance following peg‑IFN‑α therapy, were enrolled as a discovery cohort. In the discovery/screening phase, 17/20 of the randomly selected phage clones, exhibited a specific reaction with purified sera immunoglobulin G from the HBsAg clearance group, and 13/17 positive phage clones came from the same phage clone, with the inserted peptide sequence ETCRASCINESA (named IFNC1). In the validation phase, phage‑ELISA results showed that the positive reaction rate of the IFNC1 peptide phage clone was 92.0% with the HBsAg seroclearance group (n=50), which was significantly higher, as compared with the randomly selected HBsAg non‑clearance group (12.0%, n=50) and the healthy control group (8.0%, n=50). In conclusion, the newly identified mimic peptide IFNC1 showed a high predictive validity HBsAg seroclearance in patients with CHB, following peg‑IFN‑α therapy. Therefore IFNC1 may be a potential serum biomarker, which could be used to predict the treatment outcomes of peg‑IFN‑α therapy.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: The present study aimed to identify changes in atrial gene expression induced by sevoflurane and propofol using DNA microarray. The expression profiles of GSE4386 in atrial samples, obtained from patients who had received either the anesthetic gas sevoflurane or the intravenous anesthetic propofol prior to and following off‑pump coronary artery bypass graft (CABG) surgery, were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in the sevoflurane and the propofol groups were then identified and compared. Subsequently, a functional enrichment analysis was performed for the DEGs. The interactive functional modules for common, sevoflurane‑specific and propofol‑specific DEGs were then constructed for analysis of the biological processes. The percentages of common DEGs were 31.3 (275/879) and 94.8% (275/290) in the sevoflurane group and propofol groups, respectively. The functional categories for the common, sevoflurane‑specific and propofol‑specific DEGs were similar. Overall, two, one, and one functional modules were identified for the common DEGs, propofol specific DEGs and sevoflurane specific DEGs, respectively. DEGs in the modules were involved in cellular processes, including the 'regulation of transcription' and 'regulation of cellular process', which were similar to the functional annotations for the DEGs. Therefore, sevoflurane and propofol may synergistically reduce myocardial reperfusion injury in patients undergoing off‑pump CABG surgery.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: This study was conducted to determine the mRNA and protein expression levels of peroxisome proliferator‑activated receptors (PPARs) in visceral adipose tissue, as well as serum adipokine levels, in Sprague Dawley rats. The rats were fed either a normal (control rats) or excessive (experimental rats) intake of food for 8 or 16 weeks, then sacrificed, at which time visceral and subcutaneous adipose tissues, as well as blood samples, were collected. The mRNA and protein expression levels of PPARs in the visceral adipose tissues were determined using reverse transcription-polymerase chain reaction and Western blotting, respectively. In addition, the levels of adipokines in the serum samples were determined using commercial ELISA kits. The results revealed that at 8 weeks, the mass of subcutaneous adipose tissue was higher than that of the visceral adipose tissue in the experimental rats, but the reverse occurred at 16 weeks. Furthermore, at 16 weeks the experimental rats exhibited an upregulation of PPARγ mRNA and protein expression levels in the visceral adipose tissues, and significant increases in the serum levels of CCL2 and interleukin (IL)-6 were observed, compared with those measured at 8 weeks. In conclusion, this study demonstrated that the PPARγ expression level was likely correlated with serum levels of CCL2 and IL-6, molecules that may facilitate visceral adipose tissue accumulation. In addition, the levels of the two adipokines in the serum may be useful as surrogate biomarkers for the expression levels of PPARγ in accumulated visceral adipose tissues.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Pseudomonas aeruginosa continues to be a predominant cause of infections with high intrinsic resistance to antibiotics, resulting in treatment failure. P. aeruginosa is the leading cause of respiratory infections among cystic fibrosis (CF) patients. Resistance to carbapenem antibiotics among P. aeruginosa has been reported. Thus, this study was undertaken to characterize the metallo‑β‑lactamase (MBL) production of P. aeruginosa by phenotypic and genotypic methods. A total of 572 sputum samples were collected from cystic fibrosis patients along with the patient demographic details in a questionnaire. In total, 217 P. aeruginosa isolates were collected and an antibiogram revealed that 159 (73.3%) and 141 (64.9%) of these colonies exhibited resistance to imipenem and meropenem, respectively. Ceftazidime and tobramycin resistance were both identified in 112 (51.6%) isolates, and resistance to piperacillin‑tazobactam, gatifloxacin and netilmicin was detected in 96 (44.2%) respective samples. A total of 62 (28.6%) respective samples were resistant to cefoperazone, cefepime and ceftriaxone. The least antibiotic resistance was shown to amikacin and ceftizoxime with 51 (23.5%) and 32 (14.7%) respective colonies resistant to the antibiotics. The minimum inhibitory concentration (MIC) for imipenem revealed a reduction in the MIC values. MBL screening by the zone enhancement method using ceftazidime plus EDTA discs demonstrated that 63 (56.25%) of the colonies were positive for MBL. A total of 53 (84.1%) samples expressed blaVIM and 48 (76.1%) expressed blaIMP genes, as detected by duplex polymerase chain reaction. In conclusion, carbapenem resistance is of great clinical concern in cystic fibrosis patients with P. aeruginosa infection. Therefore, mandatory regular screening and monitoring the resistance in P. aeruginosa among CF patients is required.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: microRNA (miR)‑22 has been reported to be downregulated in hepatocellular, lung, colorectal, ovarian and breast cancer, acting as a tumor suppressor. The present study investigated the potential effects of miR‑22 on gastric cancer invasion and metastasis and the molecular mechanism. miR‑22 expression was examined in tumor tissues of in 89 gastric cancer patients by in situ hybridization (ISH) analysis. Additionally, the association between miR‑22 levels and clinicopathological parameters was analyzed. A luciferase assay was conducted for target identification. The ability of invasion and metastasis of gastric cancer cells in vitro and in vivo was evaluated by cell migration and invasion assays and in a xenograft model. The results showed that miR‑22 was downregulated in the gastric cancer specimens and significantly correlated with the advanced clinical stage and lymph node metastasis. In addition, metadherin (MTDH) was shown to be a direct target of miR‑22 and the expression of MTDH was inversely correlated with miR‑22 expression in gastric cancer. Ectopic expression of miR‑22 suppressed cell invasion and metastasis in vitro and in vivo. The present study suggested that miR‑22 may be a valuable prognostic factor in gastric cancer. miR‑22 inhibited gastric cancer cell invasion and metastasis by directly targeting MTDH. The novel miR‑22/MTDH link confirmed in the present study provided a novel, potential therapeutic target for the treatment of gastric cancer.
    Molecular Medicine Reports 10/2014;
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    ABSTRACT: Tissue factor (TF)/VIIa/protease‑activated receptor 2 (PAR2) has been shown to trigger the ERK1/2 signaling pathway. This was shown to be closely associated with the proliferation and migration of SW620 colon cancer cells; however, the detailed mechanisms remain unclear. The aim of the present study was to elucidate the effects of calcium signaling on the proliferation and migration of SW620 cells induced by coagulation factor VIIa. The results demonstrated that VIIa and PAR2 agonist PAR2‑AP increased [Ca2+]i in SW620 cells. In addition, VIIa‑and PAR2‑AP‑induced ERK1/2 activation was inhibited by thapsigargin (TG)‑induced depletion of intracellular Ca2+ stores and EGTA‑mediated removal of extracellular Ca2+. It was also identified that VIIa and PAR2‑AP‑induced proliferation and migration of SW620 cells was modulated by EGTA and TG. Taken together, the present results indicate that VIIa triggers calcium signaling in SW620 cells, in a TF‑dependent manner, which is critical for VIIa‑induced ERK1/2 activation in SW620 cells. These results suggested that calcium signaling had a vital role in the proliferation and migration of SW620 cells.
    Molecular Medicine Reports 10/2014;