No abstract

There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collected and the expression level of miR‑130b was determined. The online miRNA database was then searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene. Linear analysis and a luciferase assay were performed to understand the regulatory association between miR‑130b and phosphatase and tensin homolog (PTEN). In addition, reverse transcription‑polymerase chain reaction and western blot analyses were performed to examine the mRNA and protein expression levels of PTEN among individuals with lupus nephritis (n=28) and those without lupus nephritis (n=31), and in mesangial cells treated with scramble control, miR‑130b mimics, PTEN small interfering (si)RNA and miR‑130b inhibitors. In addition mesangial cells were treated with scramble control, miR‑130b mimics, PTEN siRNA and miR‑130b inhibitors to investigate the affect of miR‑130b and PTEN on the viability and apoptosis of mesangial cells. The results demonstrated that miR‑130b was downregulated in the hormone‑resistant group of lupus nephritis patients. PTEN was a virtual target of miR‑130b. There was a negative regulatory association between miR‑130b and PTEN. The mRNA and protein expression levels of PTEN were increased in the hormone‑resistant group. miR‑130b decreased the expression of PTEN. miR‑130b negatively interfered with the viability of mesangial cells and PTEN positively interfered with the viability of mesangial cells. miR‑130b accelerated apoptosis and PTEN inhibited apoptosis. Taken together, the results showed that miR‑130b was upregulated in the lupus nephritis group. PTEN was a virtual target of miR‑130b, and there was a negative regulatory association between miR‑130b and PTEN. miR‑130b and PTEN interfered with the viability and apoptosis of the mesangial cells.

Rs2910164 is associated with the risk of LN and could function as a therapeutic target of the disease.

No abstract

This study aims to explore the role and the possible underlying molecular mechanism of SNF5 in the pathogenesis of rheumatoid arthritis (RA). MH7A cells were respectively transfected with pc-SNF5 (pcDNA3.1 containing the Brg1 coding sequence), short hairpin RNA against SNF5 (shSNF5), and their negative controls (pcDNA3.1 and shNC). The alterations of SNF5 expression were assessed by qRT-PCR and western blot analysis. MTT assay, flow cytometry, and western blot analysis were performed to evaluate proliferation, apoptosis, and expression levels of p16 and JNK pathway associated proteins, respectively. Finally, the effect of SNF5 was verified in fibroblast-like synoviocytes (FLSs) obtained from a rat model with adjuvant-induced arthritis. Results showed that the expression of SNF5 was increased in the pc-SNF5 group (P < 0.05) while it was decreased in the shSNF5 group (P < 0.05). Afterwards, cell viability after transfection was reduced by SNF5 overexpression (P < 0.05, P < 0.01, or P < 0.001), whereas it was enhanced by SNF5 knockdown (P < 0.05 or P < 0.001). In terms of apoptosis, SNF5 overexpression promoted cell apoptosis (P < 0.01). The western blot analysis showed that the phosphorylated levels of proteins involved in the JNK pathway were downregulated by SNF5 overexpression while they were upregulated by SNF5 knockdown (P < 0.05, P < 0.01, or P < 0.001). However, the effect of SNF5 on the expression of p16 was the opposite. Finally, the effect of SNF5 was validated in murine FLSs. In conclusion, SNF5 suppresses proliferation and induces apoptosis of fibroblast-like cells through overexpression of p16 and suppression of the JNK pathway.