Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters










Database
Language
Publication year range
2.
Mol Med Rep ; 20(6): 4843-4854, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31661144

ABSTRACT

MicroRNAs serve an important role in the development of several diseases. Numerous genes regulate the skeletal muscle differentiation of C2C12 myoblasts. The role of miR­760 in rheumatoid arthritis (RA) has not been reported, to the best of our knowledge. Therefore, the aim of the present study was to examine the role of miR­760 in regulating skeletal muscle proliferation in RA. Potential genes functionally involved in the tarsal joint of a collagen­induced RA model were identified using Gene Expression Omnibus. Reverse transcription­quantitative PCR and western blot analyses were performed to determine the mRNA and protein expression levels. The proliferation, cell cycle progression and migration of C2C12 myoblasts were detected using Cell Counting Kit­8, flow cytometry and wound­healing assays, respectively. TargetScan was used to predict the potential target genes of miR­760, and this was verified using a dual­luciferase reporter assay. In the present study, myosin­18b (Myo18b) expression was determined to be downregulated in the RA model. Silencing Myo18b decreased the proliferation, abrogated the cell cycle progression, and reduced the migration and differentiation of C2C12 myoblasts. Expression levels of cyclin­dependent kinase 2, cyclin D1, matrix metalloproteinase (MMP)­2, MMP­9, myogenin and myosin heavy chain 6 were all decreased when Myo18b was silenced. Furthermore, overexpression of Myo18b induced opposing effects on C2C12 myoblasts. It was shown that Myo18b was a target gene of miRNA­760. Overexpression of miR­760 decreased proliferation, cell cycle progression, migration and differentiation in C2C12 myoblasts, and decreased the expression of Myo18b. The opposite results were observed when miR­760 was downregulated. In conclusion, miR­760 inhibited proliferation and differentiation by targeting Myo18b in C2C12 myoblasts. The results of the present study may contribute to understanding the mechanisms underlying RA skeletal muscle proliferation, and miR­760/Myo18b may serve as potential targets for treating patients with RA.


Subject(s)
Arthritis, Rheumatoid/genetics , Myoblasts/pathology , Animals , Arthritis, Rheumatoid/chemically induced , Arthritis, Rheumatoid/pathology , Cell Cycle , Cell Line , Cell Movement , Cell Proliferation , Collagen , Down-Regulation , Mice , Muscle Development , Myoblasts/cytology , Up-Regulation
3.
Int J Colorectal Dis ; 32(3): 433-435, 2017 Mar.
Article in English | MEDLINE | ID: mdl-28035462

ABSTRACT

OBJECTIVE: Bactericidal/permeability increasing protein (BPI) gene polymorphisms have been extensively investigated in terms of their associations with inflammatory bowel disease (IBD), with contradictory results. The aim of this meta-analysis was to evaluate associations between BPI gene polymorphisms and the risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC). METHODS: Eligible studies from PubMed, Embase, and Cochrane library databases were identified. RESULTS: Ten studies (five CD and five UC) published in five papers were included in this meta-analysis. G645A polymorphism was associated with a decreased risk of UC in allele model, dominant model, and homozygous model. CONCLUSIONS: Our data suggested that BPI G645A polymorphism was associated with a decreased risk of UC; the BPI G645A polymorphism was not associated with the risk of CD.


Subject(s)
Antimicrobial Cationic Peptides/genetics , Blood Proteins/genetics , Genetic Predisposition to Disease , Inflammatory Bowel Diseases/genetics , Polymorphism, Single Nucleotide/genetics , Case-Control Studies , Colitis, Ulcerative/genetics , Crohn Disease/genetics , Humans , Publication Bias
4.
Oncol Lett ; 11(4): 2651-2653, 2016 Apr.
Article in English | MEDLINE | ID: mdl-27073533

ABSTRACT

The typical breakpoint cluster region/Abelson (BCR-ABL) fusion gene, which is located in the Philadelphia chromosome, in association with a complex translocation event is only observed in 2-10% of patients with chronic myelogenous leukemia (CML). CML is diagnosed based on the presence of splenomegaly, increased peripheral white blood cells and the expression of BCR-ABL. The present study reports the case of a patient with CML that possessed complex aberrations involving 5 chromosome translocations, which consisted of t(1;6)(p36.1;q25) and t(9;22;11)(q34;q11.2;q11). After 2 months of follow-up, the patient is in remission following treatment with imatinib (400 mg/day) and hydroxyurea (3,000 mg/day). The hematological parameters of the patient were significantly improved and the white blood cell count returned to normal (from 361.00×109 cells/l to 6.83×109cells/l; normal range, 3.50-9.50×109 cells/l). The results of the ultrasonic examination revealed that the presence of splenomegaly had disappeared, indicating that the treatment strategy was effective. According to the outcome of the treatment, hydroxyurea in combination with imatinib is recommended for use in similar cases of CML.

SELECTION OF CITATIONS
SEARCH DETAIL
...