Shandong Univ, Shandong Prov Hosp, Dept Nephrol, Jinan, Peoples R ChinaTaishan Med Univ, Sch Basic Med, Tai An, Shandong, Peoples R ChinaShandong Univ, Shandong Prov Hosp, Dept Rheumatol, Jinan, Peoples R China
刊名
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
Lupus nephritis (LN) is a typical characteristic of systemic lupus erythematosus. MicroRNAs (miRs) are reported to be involved in the onset and development of LN. The major purpose of the current study was to uncover the function of miR-9 in the pathogenesis of LN. Expression statuses of miR-9 and its potential target, STK3 in clinical samples were investigated. Then a dual firefly luciferase assay was conducted to reveal the regulating pattern of miR-9 on STK3. Human renal mesangial cells (HMCs...更多
Lupus nephritis (LN) is a typical characteristic of systemic lupus erythematosus. MicroRNAs (miRs) are reported to be involved in the onset and development of LN. The major purpose of the current study was to uncover the function of miR-9 in the pathogenesis of LN. Expression statuses of miR-9 and its potential target, STK3 in clinical samples were investigated. Then a dual firefly luciferase assay was conducted to reveal the regulating pattern of miR-9 on STK3. Human renal mesangial cells (HMCs) were employed to detect the effect of miR-9 down-regulated expression on viability and apoptosis in nephritis cells. The mechanism of miR-9 affecting LN was explored by measuring activities of STK3, ERK, JNK, and p38 in HMCs. It was found that miR-9 level was positively correlated with LN occurrence while STK3 was negatively correlated. Firefly luciferase assay demonstrated a negative regulation of miR-9 on STK3 transcription. Reduction of miR-9 significantly down-regulated cell viability and induced apoptosis in nephritis cells. The phenotypic changes in HMCs were accompanied by suppression of all the four studied indicators. The promoting function of miR-9 on LN was firstly elucidated in our study, and the molecule mechanism was the directly inhibition of STK3 transcription, which subsequently deactivated the downstream MAPKs.收起
