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Fig. 3 | Biology Direct

Fig. 3

From: ACSM5 inhibits ligamentum flavum hypertrophy by regulating lipid accumulation mediated by FABP4/PPAR signaling pathway

Fig. 3

Overexpression of ACSM5 inhibited FABP4/PPAR signaling pathway in FFA-induced LF cells. (A) Volcano plot showed the mRNAs expression profile between FFA + ADV-NC group and FFA + ADV-ACSM5 group in LF cells. |FC| > 1.2 and FDR < 0.05 were used to screen differential expressed mRNAs. (B) The cluster heatmap showed the differential mRNA expression profiles between FFA + ADV-NC group and FFA + ADV-ACSM5 group in LF cells. (C) KEGG enrichment analysis was performed on the differential expressed genes between FFA + ADV-NC group and FFA + ADV-ACSM5 group in LF cells. (D) The differential expressed genes enriched in PPARγ signaling pathway were analyzed by PPI network. (E) ADV-ACSM5- or ADV-NC-infected LF cells were treated with FFA for 48 h, and the mRNA expression of FABP4 in LF cells was detected by RT-qPCR. (F) ADV-ACSM5- or ADV-NC-infected LF cells were treated with FFA for 48 h, and the protein expression levels of FABP4 in LF cells were detected by western blot. (G) ADV-ACSM5- or ADV-NC-infected LF cells were treated with FFA for 48 h, and the mRNA expression levels of PPARγ in LF cells were detected by RT-qPCR. (H) ADV-ACSM5- or ADV-NC-infected LF cells were treated with FFA for 48 h, and the protein expression levels of PPARγ in LF cells were detected by western blot. LF, ligamentum flavum. FFA, free fatty acids. ADV, adenovirus. NC, negative control. n.s.P > 0.05, #P < 0.05, ##P < 0.01, and ###P < 0.001

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