Skip to main content
Fig. 2 | Respiratory Research

Fig. 2

From: TNKS1BP1 mediates AECII senescence and radiation induced lung injury through suppressing EEF2 degradation

Fig. 2

IR promotes senescence of AECII induced by high expression of TNKS1BP1 could activate fibroblasts and macrophages. (A), P21 and P16 expression level on AECII Cells after over-expression TNKS1BP1 with 4 μg plasmid transfected. (B), the quantification of (A). (C), α-SMA expression level on HLF-1 Cells after co-cultured with conditioned medium from overexpression TNKS1BP1 AECII. (D), the quantification of (C). (E), iNOS expression level on RAW264.7 Cells after co-cultured with conditioned medium from overexpression TNKS1BP1 AECII. (F), the quantification of (E). (G), P21 and P16 expression level on AECII Cells after inhibition of TNKS1BP1 simultaneously under IR. (H), the quantification of (G). (I), senescence-associated secretory phenotype (SASP) related inflammatory factors (IL-1β and IL-6) on ACEII Cells after inhibition of TNKS1BP1 simultaneously under IR. (J), α-SMA expression level on HLF-1 Cells after co-cultured with conditioned medium from AECII in different treatment. (K), the quantification of (J). (L), iNOS expression level on RAW264.7 Cells after co-cultured with conditioned medium from AECII in different treatment. (M), the quantification of (L). Data are presented as mean ± SD. For statistical analysis, B, D and F were conducted by unpaired Student’s t test; H, I, K and M were conducted by One-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001 mean the difference statistical significance

Back to article page