Fig. 4 | Scientific Reports

Fig. 4

From: Decreased ALKBH5 in neutrophil correlates with disease activity in rheumatoid arthritis and ALKBH5 modulates neutrophil autophagy

Fig. 4

(A) ALKBH5 inhibited the autophagy of neutrophil through targeting ATG7 mRNA. After RIP-Seq (original blots/gels are presented in Supplementary Fig. 4), GO and KEGG analysis showed the genes exhibiting specific binding to ALKBH5 involved in autophagy. (B) Sh-ALKBH5 resulted in a rise of ATG7 mRNA level in HL-60. (C) Sh-ALKBH5 resulted in a rise of total m6A level in HL-60. (D) MeRIP-qPCR showed sh-ALKBH5 markedly induced the m6A level of ATG7 mRNA. (E) Actinomycin D treatment indicated the ATG7 mRNA decay rate of sh-ALKBH5 was slower than that of sh-GFP. (F) The mRNA expression of ATG7 in neutrophil from RA patients was significantly increased than that in HC. (G) The mRNA expression of ATG7 negatively correlated with the mRNA expression of ALKBH5 in neutrophil from RA patients. ALKBH5: alkylation repair homolog protein 5, ATG7: Autophagy related 7, HC: health control, MeRIP-qPCR: m6A immunocoprecipitation-quantitative polymerase chain reaction, RA: rheumatoid arthritis, RIP-Seq: RNA immunoprecipitation with next generation sequencing.

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