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. 2023 Apr 20;16:1153870. doi: 10.3389/fnmol.2023.1153870

Figure 2.

Figure 2

Downregulation of cingulate PRMT1 was sufficient and necessary for the development of peripheral hypersensitivity (A) Up: schematics of lentivirus vector engineered shRNA to knock down Prmt1 and eGFP control (Ctrl). Bottom: the experimental paradigm for behavioral testing. scale bar, 200 μm. (B) Illustration of bilateral expression of lenti-Prmt1 in C57BL/6 J mouse ACC. (C) PWT tests after Prmt1 shRNA expressed in the ACC (two-way RM ANOVA, interaction: F(2;36) = 23.95, p < 0.01, Time: F(2;36) = 16.95, p < 0.01, Ctrl vs. shRNA: F(1;36) = 152.63, p < 0.01, Ctrl: n = 10, shRNA: n = 10; “**” indicates p < 0.01; BL: baseline). (D) Statistics for the center time in the open-field test (Ctrl: n = 5, shRNA: n = 4, unpaired t-test, p > 0.05). (E) Statistics for the total distance in the open-field test (Ctrl: n = 5, shRNA: n = 4, unpaired t-test, p > 0.05). (F) Western blots and quantification showing efficient knockdown of PRMT1 by shRNA in the ACC (Ctrl: n = 5, shRNA: n = 4, unpaired t-test, p = 0.0039; “**” indicates p < 0.01). (G) Example injection site of cannula in the ACC of C57BL/6 J mice. (H) PWT tests after micro infusion of PRMT1 inhibitor, AMI-1, into ACC (Two-way RM ANOVA, interaction: F (1;9) = 10.19, p < 0.05, Time: F (1;9) = 13.51, p < 0.05, saline vs. AMI-1: (F) (1;9) = 7.24, p < 0.05, Ctrl: n = 6, AMI-1: n = 5; “*” indicates p < 0.05). Data are represented as mean ± SEM; ns, not significant.