Fig 1: The absence of Crp3 blunts the proteolytic profile of aortic SMCs. (A) Quantitative analysis of the secretion and activation of Mmp-2 in the media of control and IL-1β-stimulated aortic SMCs. IL-1β increased Mmp-2 activation, a response that was attenuated in Crp3−/− SMCs (WT n = 4, Crp3−/− n = 5). ** indicates p = 0.027 (B) Total Mmp-2 levels remained unchanged (WT n = 6, Crp3−/− n = 7). (C) The secretion of Mmp-9 was induced by IL-1β in WT, but not in Crp3−/− SMCs (WT n = 8, Crp3−/− n = 5). ** indicates p = 0.0048, *** indicates p < 0.001 (D) Secreted Timp-2 levels remained unchanged in response to IL-1β in WT and Crp3−/− SMCs (WT n = 7, Crp3−/− n = 7). (E) The collagenase activity was induced by IL-1β in WT, but not in Crp3−/− SMC (WT n = 17, Crp3−/− n = 17). *** indicates p = 0.0009. (F) The elastolytic activity was induced by IL-1β in both WT and Crp3−/− SMC, but in a higher level in WT (WT n = 11, Crp3−/− n = 11). * indicates p = 0.0208, and **** indicates p < 0.0001.
Fig 2: Impact of Crp3 knockout in the inflammatory response. Gene expression analysis showing (A) increased expression of Mmp-9 only by wild type macrophages in response to M2 polarization, while (B) the expression of Timp-2 is upregulated in Crp3−/−, but not in wild type macrophages. (C) Mmp-2 expression levels are similar in both groups (WT n = 6, Crp3−/− n = 5). ** indicates p = 0.0017.
Supplier Page from Abcam for Rat TIMP-2 ELISA Kit