Fig 1: DPP4 increased Ip3r2 protein expression via PAR2/ERK/CEBPB/ERp29 signaling in an enzymatic activity-independent manner(A) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4, DPP4+sitagliptin, or DPP4 S624A, respectively.(B) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in the hippocampus from db/m, db/db or DPP4m db/db mice. (n = 6/group).(C) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4, DPP4 S624A, or DPP4 ?405-425, respectively.(D) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4 S624A, DPP4 S624A + siControl or DPP4 S624A + siPAR2, respectively.(E) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4 S624A or DPP4 S624A + ERKi, respectively.(F) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4 S624A, DPP4 S624A + siControl or DPP4 S624A + siCEBPB, respectively.(G) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in primary hippocampal neurons treated with DPP4 S624A, DPP4 S624A + siControl or DPP4 S624A + siERp29, respectively.(H) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in the hippocampus from DPP4m db/db, DPP4m db/db+shControl, or DPP4m db/db+shPAR2 mice. (n = 6/group).(I) Immunoblots and quantification analysis of protein levels of p-ERK1/2, ERK, p-CEBPB, CEBPB, ERp29, and IP3R2 in the hippocampus from DPP4m db/db, DPP4m db/db+shControl, or DPP4m db/db+shERp29 mice. (n = 6/group).
Fig 2: The non-canonical function of DPP4 promotes MAM formation, mitochondrial calcium overload, mitochondrial dysfunction, and cognitive impairment via PAR2/ERK/CEBPB/ERp29 signaling(A–D) Representative TEM images of the ER and mitochondrial morphology (Scale bar, 1 µm) (A), FCM analysis of mitochondrial calcium levels (B), MPTP opening (C), and MMP (D) in primary hippocampal neurons under different treatments. (Samples: (I) control, (II) DPP4, (III) DPP4 S624A, (IV) DPP4 ?405-425, (V) DPP4 S624A + PAR2siRNA, (VI) DPP4 S624A + ERKi, (VII) DPP4 S624A + CEBPBsiRNA, (VIII) DPP4 S624A + ERp29siRNA).(E) Morris water maze behavioral assessment for mice under different treatments. (Samples: (I) db/m, (II) db/db, (III) DPP4m db/db, (IV) DPP4m db/db+shPAR2, (V) DPP4m db/db+shCEBPB, (VI) DPP4m db/db+shERp29) showing differences in path (upper panel), escape latency (bottom left panel), the time mice stayed in the target quadrant (bottom middle panel) and number of times mice passed through the platform location in the probetrial (bottom right panel) during the learning session. (n = 6/group).
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