@article {Xiao:2015:1791-2997:2765,
title = "Inhibiting Notch1 reduces the expression of Tolllike receptor9 in BABL/Clpr mouse kidneys and improves glucocorticoid sensitivity",
journal = "Molecular Medicine Reports",
parent_itemid = "infobike://sp/mmr",
publishercode ="sp",
year = "2015",
volume = "12",
number = "2",
publication date ="2015-08-01T00:00:00",
pages = "2765-2770",
itemtype = "ARTICLE",
issn = "1791-2997",
eissn = "1791-3004",
url = "https://www.ingentaconnect.com/content/sp/mmr/2015/00000012/00000002/art00157",
doi = "doi:10.3892/mmr.2015.3758",
author = "Xiao and Ning and Zhang and Wu and Zuo",
abstract = "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 receptor9 (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.",
}