Figure 2.

Suppression of CRISPLD2 in MRC5CRISPLD2KD exacerbated lipopolysaccharide (LPS)‐induced inflammation. MRC5CRISPLD2KD and MRC5control were grown to 80% confluence in 6‐well plates, and treated with LPS 1 μg/mL in serum‐contained medium EMEM for 24 h. Cells were collected for RNA isolation and RT‐PCR. Expression of IL‐8 and CCL‐2 were assessed by q‐PCR (n = 4, *P < 0.05, **P < 0.01 in treatment with LPS vs. no LPS, #P < 0.05 in MRC5CRISPLD2KD vs. MRC5control by two‐way analysis of variance [ANOVA]). Secretion of IL‐8 into supernatant was assessed by ELISA. (n = 3, *P < 0.05, fold change over the base: MRC5 control without LPS; #P < 0.05 in MRC5CRISPLD2KD vs. MRC5control by two‐way ANOVA).