Aims: Abnormal expression of long non-coding RNAs (lncRNAs) occurs in several diseases including renal fibrosis. Notably, growth arrest-specific 5 (Gas5) is a lncRNA, which functions as an essential modulator of cell proliferation and growth. However, the role and expression of lncRNA Gas5 associated with renal fibrosis remains controversial. Herein, we investigate the effect of lncRNA Gas5 deficiency in renal fibrosis induced by the operation of unilateral ureteric obstruction (UUO) in mice.
Main methods: Sera and urine of mice were used to detect markers of renal function. Further, Masson and immunohistochemical staining, western blotting as well as qRT-PCR were performed to observe the distribution and expression of fibrosis marker in the kidney tissue of the mice.
Key findings: Unlike the wild type mice, the obstructed kidney in Gas5+/- mice showed more severe renal fibrosis and collagen deposition. In the UUO-Gas5+/- group, the serum levels of uric acid, serum creatinine, and the urine levels of albumin-to-creatinine ratio were higher. Moreover, the expression of mRNA and protein of α-smooth muscle actin (α-SMA), vimentin, collagen IV, fibronectin, and matrix metalloproteinase 9 (MMP9) were higher, whereas that of phosphatase and tensin homolog (PTEN) were lower with the difference being statistically significant (p < 0.05).
Significance: lncRNA Gas5 was up-regulated in renal fibrosis tissues, and its deficiency exacerbated renal fibrosis in the UUO mice model.
Keywords: Growth arrest-specific 5; Long noncoding RNAs; Renal fibrosis; Renal function; Unilateral ureteral obstruction.
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