miR-218 expression in osteosarcoma tissues and its effect on cell growth in osteosarcoma cells

Objective:To investigate the expression of miR—218 and its clinical significance in osteosarcoma tissues and explore its effect on proliferation and apoptosis in osteosarcoma cells.Methods:miR-218 expression was detected in 76 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues using quantitative reverse transcription polymerase chain reaction(qRT-PCR).MiR-218 was over-expressed by exogenous miR-218 plasmids in Saos-2 cells,and then BrdU cell proliferation assay and flow cytometry were used to determine cell proliferation and apoptosis.Results:The expression of miR-218 in osteosarcoma tissues was significantly lower than those in normal tumor-adjacent tissues(t=8.735.P<0.001).MiR-218 expression in tumor tissues was significantly correlated with tumor size(x^2=5.380,P=0.020).clinical stage(x^2=6.692,P=0.010) and distant metastasis(x^2=4.l80.P=0.041).MiR-218 was obviously overexpressed by exogenous miR-218 plasmids(t= 19.42.P<0.001),and miR-218 overexpression significantly reduced cell proliferation(t=9.045.P<0.001) and induced apoptosis(t=12.38,P<0.001) in Saos-2 cells.Conclusions:The low-expression of miR-218 is correlated with the poor clinicopathological features in osteosarcoma.Moreover.miR-218 overexpression reduces cancer cell proliferation and induces apoplosis in Saos-2 cells,suggesting that miR-218 may play a key role in the progression of human osteosarcoma.

Role of immune dysfunction in pathogenesis of type 1 diabetes mellitus in children

Objective:To investigate the function of cytokines,chemokines,and regulatory T cells(Tregs)in the pathogenesis of Type 1 diabeles mellitus(T1DM)in children.Methods:A total of 35 children with T1DM and 30 healthy controls were enrolled in this study.Levels of serum cytokines(IL-1α,IL-6,IL-10,IL-12,and TNF-α)and chemokines(MIP-1α,MIP-1βand MCP-1)were detected by enzyme-linked immunosorbent assay.Peripheral blood mononuclear cells(PBMCs)were isolated and culture supernatant of phytohaemagglutinin(PHA)-stimulatcd PBMCs was subjecled to ELISA for levels of cytokines(IL-1α,IL-6,IL-10,IL-12 and TNV-α)in T1DM and control group.Furthermore,flow cytometty was used to determine the percentage of Tregs in PBMCs of two groups.Results:Levels of serum cytokines including IL-1α,IL-6,IL-10 andd TNF-αas well as chemokines,such as MIP-1αand MIP-1βin children with T1DM children were significantly higher than those in healthy controls(P<0.05,respectively).PBMCs with PHA stimulation in T1DM group secreted more IL-1αand TNF-α(P<0.05,respectively),but less IL-10(P<0.05),as compared with control group.Furthermore,the proportion of CD4^+,CD25^+,Foxp3.Tregs in PBMCs isolated from children with T1DM was obviously lower than those in heathy controls(P<0.05).Conclusions:Immune dysfunction.with uprcgulation of inflanunatory factors such as IL-1α.IL-6.TNF-αand MIP-1α.downregulation of IL-10 and Tregs,plays an important role in the pathogenesis of T1DM in children.

Glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor regulate the interaction between astrocytes and Schwann cells at the trigeminal root entry zone

The trigeminal root entry zone is the zone at which the myelination switches from peripheral Schwann cells to central oligodendrocytes.Its special anatomical and physiological structure renders it susceptible to nerve injury.The etiology of most primary trigeminal neuralgia is closely related to microvascular compression of the trigeminal root entry zone.This study aimed to develop an efficient in vitro model mimicking the glial environment of trigeminal root entry zone as a tool to investigate the effects of glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor on the structural and functional integrity of trigeminal root entry zone and modulation of cellular interactions.Primary astrocytes and Schwann cells isolated from trigeminal root entry zone of postnatal rats were inoculated into a two-well silicon culture insert to mimic the trigeminal root entry zone microenvironment and treated with glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor.In monoculture,glial cell line-derived neurotrophic factor promoted the migration of Schwann cells,but it did not have effects on the migration of astrocytes.In the co-culture system,glial cell line-derived neurotrophic factor promoted the bidirectional migration of astrocytes and Schwann cells.Brain-derived neurotrophic factor markedly promoted the activation and migration of astrocytes.However,in the co-culture system,brain-derived neurotrophic factor inhibited the migration of astrocytes and Schwann cells to a certain degree.These findings suggest that glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor are involved in the regulation of the astrocyte-Schwann cell interaction in the co-culture system derived from the trigeminal root entry zone.This system can be used as a cell model to study the mechanism of glial dysregulation associated with trigeminal nerve injury and possible therapeutic interventions.

MMP-9 deficiency accelerates the progress of periodontitis

Periodontitis is a chronic inflammatory disease caused by periodontopathic bacteria that affects periodontal support tissues.1 If left untreated,it results in loss of periodontal attachment and alveolar bone resorption.Approximately one-half of adults in the United States older than 30 years have periodontal disease.2 Though the disease is initiated by bacterial infection,it activates host defense systems that eventually lead to the degradation of the periodontium.During periodontitis,the disease progress involves further production of pro-inflammatory mediators such as cytokines,proteolytic enzymes like matrix metalloproteinases(MMPs),and their inhibitors.