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. Author manuscript; available in PMC: 2008 Apr 3.
Published in final edited form as: Nat Med. 2008 Feb 10;14(3):331–336. doi: 10.1038/nm1723

Figure 2. MMP-9 is both required and sufficient for producing neuropathic pain symptom.

Figure 2

(a) Persistent infusion of MMP-9 inhibitor delays the development of mechanical allodynia in SNL rats. The inhibitor or vehicle (20% DMSO) was intrathecally infused via an osmotic pump (0.5 μl/h, 7 days) starting 2 days before SNL (* p<0.05, compared to corresponding vehicle control, n=6). BL indicates baseline. (b) Reversal of mechanical allodynia by endogenous MMP-9 inhibitor TIMP-1 in SNL rats (* p<0.05, compared to saline, n=6). (c) Pretreatment of MMP-9 siRNA (2 × 5 μg, i.t.) delays the development of mechanical allodynia in SNL rats (* p<0.05, compared to respective mismatch control RNA, n=9). Insert, gelatin zymography showing knockdown of MMP-9 but not MMP-2 by MMP-9 siRNA in the DRG on SNL day 1. (d) Intrathecal administration of MMP-9 induces rapid but reversible mechanical allodynia in rats (* p<0.05, compared to saline control, n=12). (e) MMP-9 null mice show a reduction in SNL-induced spontaneous pain at early times (* p<0.05, compared to wild type mice, n=6). Spontaneous pain was evaluated by counting the number of flinches of affected hindpaws over a 2-minute period. (f) MMP-9 null mice show a reduction of mechanical allodynia at early times after SNL (* p<0.05, compared to wild type mice, n=6). Insert, gelatin zymography showing absence of MMP-9 in MMP-9 null mice.