p38 MAPK regulates LAMP2A-mediated CMA in microglia cells. A) Microgila cells were isolated from the rats of different groups, and immunoblot of LAMP2A in the total cell lysate or lysosome of LAMP2A, β-actin and Hsc70 were used as loading control, respectively, and analysis of densitometric quantification of LAMP2A according to immunoblotting. Representative blots were from n = 3. B) Immunoblot of LAMP2A in the lysosome of LAMP2A in microgila cells with different treatment, and densitometric quantification of LAMP2A according to immunoblotting. Representative blots were from n = 3. C) Immunofluorescence of DAPI, p-p38 and LAMP1 with microgila cells isolated from the spinal cord injured site of sham or SCI group. Representative images were from n = 3. Scale bar, 50 μm. D) Denstimetric quantification of immunofluorescent density based on (C). E) Immunoblot of LAMP2A, CD63 and LAMP1 in the lysosome of microgila cells with different treatment. Representative blots were from n = 3. F) Densitometric quantification of LAMP2A and CD63 according to immunoblotting. G) Immunoblot of LAMP2A and Cath B in the lysosome of microgila cells with different treatment (left panel), and densitometric quantification of LAMP2A according to immunoblotting. Representative blots were from n = 3. H) Detecting of Rnase A by native-PAGE in microgila cells with different treatment (lower panel) and densitometric quantification of Rnase A according to immunoblotting (upper panel). n = 3. ^*P < 0.05 compared to control and sham; ^**P < 0.01 compared to control and sham; ^***P < 0.001 compared to sham. #P < 0.05 compared to SCI; ##P < 0.01 compared to SCI. 2-way ANOVA following Tukey’s multiple comparisons test.