Based on the important functions of phosphatase and tensin homolog (PTEN)-Long for renal diseases, the present study aimed to investigate the expression of PTEN-Long in patients and mice with nephritis and its effect on nephritis. Expression levels of PTEN-Long in serum of patients with nephritis, renal cell carcinoma (RCC) as well as normal controls, and in serum and renal tissues of mice were measured by western blotting. PTEN-Long knock-in and knock-out mice were constructed via the CRISPR-Cas9 technique. Intraperitoneal injection of lipopolysaccharide+renal homogenate was performed to construct a mouse nephritis model. Mice were divided into control group, model group, knock-in group and knock-out group. A Bio-Plex system was used to detect secretion of serum inflammatory factors. Expression of inflammatory factors in renal tissues of different groups was detected by reverse transcription semi-quantitative polymerase chain reaction. Hematoxylin and eosin staining was used to observe the pathological changes of renal tissue. PTEN-Long was downregulated in patients with nephritis and RCC compared with controls, whereas the expression levels of inflammatory factors were increased. PTEN-long knock-in significantly reduced the serum content and expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18. PTEN-long knock-out also decreased the expression levels of TNF-α and IL-6 but exhibited no effects on expression of IL-1β and IL-18. Compared with knock-out and model groups, renal tissue inflammation was significantly reduced in knock-in group. The protein level of PTEN-Long was significantly lower in serum than in renal tissue. These findings suggest that PTEN-long can inhibit the progression of nephritis by interacting with inflammatory factors to protect kidney.
Keywords: inflammatory factors; mouse nephritis model; nephritis; pathological changes; phosphatase and tensin homolog-Long.