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308 Study on the role of microrna125a in lupus disease in mice
  1. H Qin1
  1. 1Ren Ji Hospital- School of Medicine- Shanghai Jiao Tong University, Rheumatology, Shanghai, China

Abstract

Background and aims To investigate whether over-expression of miRNA125a has an effect on organic injuries and its potential mechanisms by using miRNA-125a-agomir transfected MRL/lpr mice

Methods 5-week-old female MRL/lpr and MRL/n mice were divided into three groups : the lpr-miRNA-group, given miRNA-125a-agomir intravenously ; the lpr-PBS-group, given PBS intravenously ; MRL-control-group: receiving no treatment. Blood samples and urine were collected weekly interval from 5-week-age. At 13-week-age and 17-week-age, bronchoalveolar lavage fluid, blood sample, lung and spleen tissues were collected and analysed in half of the mice.

Results MiRNA-125a levels in splenocytes were significantly elevated in MRL/lpr mice.

A variety of inflammatory cell infiltration, mostly T cells, in lung tissues was statistically alleviated in lpr-miRNA group.

Flow cytometry analysis indicated that in lpr-miRNA group, the proportion of splenic plasma cells in lpr-miRNA group was significantly decreased than that in lpr-PBS group.

Cytokines analysis showed serum levels of RANTES in lpr-miRNA group were statistically reduced.

The serum level of anti-dsDNA and the high tilter proportions of ANA were much lower in lpr-miRNA group than in lpr-PBS group.

Conclusions Intravenous injection of miRNA125a-agomir+Engreeen in vivo transfection reagent mixture solution could transfect miRNA-125a and increase the level of miRNA-125a expression safely and effectively.

Over-expression of miRNA-125a could alleviate inflammatory cell infiltration in lung tissues in lpr mice and reduce the proportion of splenic plasma cell.

Elevation of miRNA-125a expression could inhibit the expression of RANTES in lpr mice, which in turn reduce the autoimmune inflammation to a certain extent.

Over-expression of miRNA-125a could reduce serum autoantibodies and suppress autoimmune reaction in lpr mice.

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