By a News Reporter-Staff News Editor at Gene Therapy Weekly -- A new study on Autoimmune Diseases is now available. According to news reporting originating in Hiroshima, Japan, by NewsRx journalists, research stated, "MicroRNAs, a class of noncoding RNAs, play roles in human diseases. MicroRNA-223 (miR-223) is reported to play critical roles in osteoclastogenesis."
The news reporters obtained a quote from the research from Hiroshima University, "The purpose of this study was to analyze the expression pattern of miR-223 in rheumatoid arthritis (RA) synovium and examine the suppression of osteoclastogenesis from human peripheral blood mononuclear cells (PBMC) by overexpression of miR-223. Expression of miR-223 in synovium from RA patients was analyzed by quantitative reverse transcription polymerase chain reaction (RT-PCR) and section in situ hybridization. MiR-223 was overexpressed in an osteoclastogenesis coculture system with PBMC and RA synovial fibroblast. At 3 weeks after transfection of double-stranded miR-223, the formation of tartrate-resistant acid phosphatase (TRAP)-stained multinucleated cells was analyzed to evaluate the inhibitory effect of miR-223 on osteoclastogenesis. MiR-223 was more highly expressed in RA synovium than in osteoarthritis (OA) synovium due to the increased number of miR-223-positive cells in RA synovium. MiR-223 was expressed in the superficial and sublining layers, and macrophages, monocytes, and CD4 T cells also expressed miR-223. The number of TRAP-positive multinucleated cells was significantly decreased by overexpression of miR-223 in a dose-dependent manner. The expression of osteoclastogenesis marker genes was significantly down-regulated by miR-223 overexpression. MiR-223 is intensely expressed in RA synovium, and overexpression of miR-223 suppresses osteoclastogenesis in vitro."
According to the news reporters, the research concluded: "This study demonstrates the possibility of gene therapy with miR-223 to treat bone destruction in RA patients."
For more information on this research see: Overexpression of microRNA-223 in rheumatoid arthritis synovium controls osteoclast differentiation. Modern Rheumatology, 2013;23(4):674-85. Modern Rheumatology can be contacted at: Springer, 233 Spring Street, New York, NY 10013, USA. (Springer - www.springer.com; Modern Rheumatology - www.springerlink.com/content/1439-7595/)
Our news correspondents report that additional information may be obtained by contacting H. Shibuya, Programs for Applied Biomedicine, Division of Clinical Medical Science, Dept. of Orthopedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, Japan. Additional authors for this research include T. Nakasa, N. Adachi, Y. Nagata, M. Ishikawa, M. Deie, O. Suzuki and M. Ochi (see also Autoimmune Diseases).
The publisher of the journal Modern Rheumatology can be contacted at: Springer, 233 Spring Street, New York, NY 10013, USA.
Keywords for this news article include: Asia, Biotechnology, Japan, Genetics, Hiroshima, Macrophages, Osteoclasts, Gene Therapy, Bioengineering, Joint Diseases, Autoimmune Diseases, Rheumatoid Arthritis, Musculoskeletal Diseases.
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