动物造模,细胞自噬 z-bio 2022-02-01 498

　　Objective To investigate the regulatory effect and molecular mechanism of small ubiquitin-like modifier-specific protease 3 on autophagy in mouse lung tissue cells.

　　Methods Immunofluorescence technique was used to detect the location of SENP3 in lung tissue cells; wild-type C57BL/6J mice with SENP3 gene (SENP3+/+) and SENP3 knockout heterozygous mice (SENP3+/-) were starved to induce cells Autophagy; Application of immunoblotting method to assess the level of cell autophagy; Application of electron microscope observation and immunofluorescence technology to analyze the types of cells undergoing autophagy; Application of immunoprecipitation method to detect autophagy-related molecules, coiled-coil Myosin-like Bcl-2 interacting protein 1 (coiledcoil myosin-like Bcl-2-interacting protein 1, BECN1) SUMO modification.

　　Result SENP3 is highly expressed in alveolar type II epithelial cells. After the mice were starved, the alveolar type Ⅱ epithelial cells showed autophagy, and SENP3+/- mice were more obvious than SENP3+/+ mice. At the same time, the SUMO2/3 modification of BECN1 in lung tissue samples was removed by SENP3.

　　Conclusion SENP3 inhibits the autophagy of mouse alveolar type II epithelial cells under starvation stress, and can finely regulate the degree of autophagy.