Gang Li1, Zhongpeng Qiu2. 1. Department of Orthopedics, First Affiliated Hospital of Shihezi University Medical College, China Lig1993@163.com. 2. Department of Orthopedics, First Affiliated Hospital of Shihezi University Medical College, China.
Abstract
OBJECTIVE: MiR-15 is involved in modulating many cellular processes that are normally destroyed in disease. The regulation of the cell cycle, angiogenesis, and responses to cellular stress are notable processes influenced by MiR-15. MiR-15 plays a critical role in the model of inflammation-related angiogenesis defects. However, its role in rheumatoid arthritis (RA) remains unclear. In this paper, we questioned the potential effects miR-15 has on RA. METHODS: Synthetic mimics of miR-15 were transfected into human RA fibroblast-like synoviocyte (FLS) cell line MH7A cells. Cell proliferation was detected by a Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was determined by flow cytometry. MH7A cells, stimulated by interleukin-1β (IL-1β), were transfected with miR-15 mimics and inhibitors. Western blot and quantitative real time (qRT)-PCR were used to detect gene and protein expressions. Bioinformatic software analysis and luciferase reporter assays were used to predict and validate miR-15 targets. RESULTS: We found that the miR-15 experienced down-regulated expression in MH7A cells, after they were stimulated with IL-1β. MiR-15 inhibited inflammatory cell proliferation and promoted inflammatory cell apoptosis. BCL2L2 was identified as a target of miR-15 by luciferase assay. Additionally, NF-κB signaling pathway related proteins were inhibited by miR-15 overexpression. CONCLUSION: These findings contribute to an understanding of the impact that miR-15 possesses on inflammatory injury, and provide a basis for RA treatment.
OBJECTIVE: MiR-15 is involved in modulating many cellular processes that are normally destroyed in disease. The regulation of the cell cycle, angiogenesis, and responses to cellular stress are notable processes influenced by MiR-15. MiR-15 plays a critical role in the model of inflammation-related angiogenesis defects. However, its role in rheumatoid arthritis (RA) remains unclear. In this paper, we questioned the potential effects miR-15 has on RA. METHODS: Synthetic mimics of miR-15 were transfected into humanRA fibroblast-like synoviocyte (FLS) cell line MH7A cells. Cell proliferation was detected by a Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was determined by flow cytometry. MH7A cells, stimulated by interleukin-1β (IL-1β), were transfected with miR-15 mimics and inhibitors. Western blot and quantitative real time (qRT)-PCR were used to detect gene and protein expressions. Bioinformatic software analysis and luciferase reporter assays were used to predict and validate miR-15 targets. RESULTS: We found that the miR-15 experienced down-regulated expression in MH7A cells, after they were stimulated with IL-1β. MiR-15 inhibited inflammatory cell proliferation and promoted inflammatory cell apoptosis. BCL2L2 was identified as a target of miR-15 by luciferase assay. Additionally, NF-κB signaling pathway related proteins were inhibited by miR-15 overexpression. CONCLUSION: These findings contribute to an understanding of the impact that miR-15 possesses on inflammatory injury, and provide a basis for RA treatment.