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. 2014 Nov 6;4:6943. doi: 10.1038/srep06943

Figure 2. Neointima formation, cell proliferation, cell migration and inflammation in Xbp1 haploinsufficiency.

Figure 2

(A), (B). Left femoral arteries of 7-8-week-old male Xbp1+/+ (n = 7) and Xbp1+/− (n = 7) mice were subjected to wire-induced vascular injury. After 4 weeks, EVG staining was performed in the left femoral artery (A). Scale bars: 50 µm. The extent of neointima formation was evaluated as intima-to-media ratio in the wire-injured artery of Xbp1+/+ and Xbp1+/− mice (B). *P < 0.05. (C), (D). Gene expression of unfolded protein response (UPR) markers in the IRE1α-XBP1 branch (C) and the other branches (D) in Xbp1-knockdown human coronary artery smooth muscle cells (CASMC). *P < 0.05. (E). Cell proliferation was assessed by an MTS assay in Xbp1-knockdown CASMC with 20 ng/ml platelet-derived growth factor-BB (PDGF-BB) for 48 h. *P < 0.05 vs. Control-PDGF-BB(-); †P < 0.05 vs. Xbp1 KD-PDGF-BB(-); ‡P < 0.05 vs. Control-PDGF-BB(+). (F). Cell migration was assessed by a scratch wound assay in Xbp1-knockdown CASMC treated with 20 ng/ml PDGF-BB for 8 h. Photographs were taken, and migration distance was measured by ImageJ. *P < 0.05. (G). Gene expression of PDGF receptors, PDGFR-α and PDGFR-β, in Xbp1-knockdown CASMC. *P < 0.05. (H). Western blotting analysis of ER stress markers in Xbp1-knockdown CASMC treated with 20 ng/ml PDGF-BB for 48 h. (I). Gene expression of inflammatory markers, IL-1β and IL-6, in Xbp1-knockdown CASMC treated with 20 ng/ml PDGF-BB for 48 h. *P < 0.05 vs. Control-PDGF-BB(−); †P < 0.05 vs. Xbp1 KD-PDGF-BB(−); ‡P < 0.05 vs. Control-PDGF-BB(+).