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. 2022 Oct 3;12(16):6989–7008. doi: 10.7150/thno.75069

Figure 7.

Figure 7

CHI3L1 interacts with CD44 to drive M2 TAMs polarization. (A-B) Western blot of CHI3L1, p65, and ACTN4 expression after TNFɑ treatment in U87MG and A172 cells, which were pretreated with dimethyl sulfoxide (DMSO), CB, (-)-B, PF, and Y. (C-D) Cytoplasmic and nuclear CHI3L1, p65, and ACTN4 were analyzed using western blot. (E) mRNA expression levels of CHI3L1 between the control and CB pretreated group in U87MG and A172 cell lines. (F) Co-immunofluorescent staining of CHI3L1 and CD206 in frozen sections of human gliomas. (G-H) Macrophages derived from THP1 induced by PMA (10 ng/mL) for 24 h, and identified by morphologic evaluation and mRNA expression of CD68. (I) M2 markers (CD206 and CD163) expression in macrophages treated with IL-4 (100 ng/mL), rhCHI3L1 (500 ng/mL), and the culture supernatant (cs) of U87MG and A172 cells measured by IF. (J-K) mRNA expression of M1 and M2 markers quantitated by qRT-PCR in macrophages treated with IL4, and the culture supernatant of U87MG and A172 cells. (L-N) Migration of U118MG cells induced by M2 macrophages. (O-V) mRNA expression of M1 and M2 markers in Cd44+/+ and Cd44-/- BMDMs treated with IL-4 and rmCHI3L1 (500 ng/mL). (W) Western blot of phosphorylation of AKT and p38 in Cd44+/+ and Cd44-/- BMDMs pretreated with rmCHI3L1.