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Inhibiting Notch1 reduces the expression of Tolllike receptor 9 in BABL/Clpr mouse kidneys and improves glucocorticoid sensitivity

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, characterized by the development of a pathogenic autoantibodies. Lupus nephritis is a major cause of mortality in patients with SLE. Glucocorticoids are used for the treatment of lupus, however, corticosteroids have no effect on the expression of Tolllike receptor 9 (TLR9), which may limit response to corticosteroids in certain patients with SLR. The expression of TLR9 can be used as a predictor of glucocorticoid response in patients with active SLE. The present study analyzed urine proteins and pathological kidney sections of BABL/Clpr mice and found that, following the inhibition of Notch1, glucocorticoid treatment improved the symptoms of lupus nephritis. Furthermore, glucocorticoid treatment reduced the expression of TLR9 in the BABL/Clpr mouse kidneys, according to immunohistochemical and western blot analyses. These results suggested that inhibition of the expression of Notch1 enhanced corticosteroid sensitivity in BABL/Clpr mice.
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Document Type: Research Article

Affiliations: 1: Department of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China 2: Department of Chinese Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China

Publication date: August 1, 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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