动物造模 z-bio 2022-03-04 291

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

　　Methods Immunofluorescence technique was used to detect the localization of SENP3 in lung tissue cells; SENP3 gene wild-type C57BL/6J mice (SENP3+/+) and SENP3 knockout heterozygous mice (SENP3+/-) were starved to induce cells. Autophagy; Western blotting was used to assess the level of autophagy; electron microscopy and immunofluorescence techniques were used to analyze the cell types undergoing autophagy; Co-immunoprecipitation was used to detect the autophagy-related molecule coiled-coil Myosin-like Bcl-2 interacting protein 1 (coiledcoil myosin-like Bcl-2-interacting protein 1, BECN1) SUMOylation modification.

　　Results SENP3 was highly expressed in alveolar type II epithelial cells. After mice were starved, alveolar type II epithelial cells showed autophagy, and SENP3+/- mice were more pronounced 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.