期刊
BIOSCIENCE REPORTS
卷 38, 期 -, 页码 -出版社
PORTLAND PRESS LTD
DOI: 10.1042/BSR20180626
关键词
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资金
- National Natural Science Foundation of China [81402936, 81302576]
- Jiangsu Provincial Natural Science Foundation of China [BK20131234]
- six talent peak research projects in Jiangsu province [2015-WSN-105]
- 333 project of Jiangsu Province, Jiangsu Province Youth Medical Talent Project
- Jiangsu Province Clinical Medical Science and Technology Project [BL2013034]
Rheumatoid arthritis (RA) is a common chronic autoimmune joint disease characteristic of elevated proliferation and infiltration of fibroblast-like synoviocytes (FLS). Here, we aimed to explore the mechanisms of the Tanshinone IIA (Tan IIA)-induced apoptosis of FLS from patients with RA (termed RAFLS). Cell Counting Kit-8 (CCK-8) assay and Annexin V staining revealed that RAFLS viability decreased and apoptosis increased after Tan IIA treatment. Long non-coding RNA (lncRNA) GAS5 expression was significantly decreased in the synovial tissues and RAFLS, while Tan IIA treatment resulted in an up-regulation of GAS5. Consistently, knockdown of GAS5 using siRNA inhibited RAFLS apoptosis. Mechanistically, GAS5 knockdown down-regulated the expression of cleaved caspase-3 and caspase-9 in the RAFLS cells and activated the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway. These data indicate that Tan IIA promotes RAFLS apoptosis by up-regulating lncRNA GAS5, with enhanced expression of cleaved caspase-3/caspase-9 and inhibited PI3K/AKT signaling.
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