antibodies against rtn4  (Proteintech)

Journal: Redox biology

Article Title: Nogo-B mediates endothelial oxidative stress and inflammation to promote coronary atherosclerosis in pressure-overloaded mouse hearts.

doi: 10.1016/j.redox.2023.102944

Figure Lengend Snippet: Fig. 1. Nogo-B upregulated in heart tissues of ApoE¡/¡ mice after TAC. (A) Immunofluorescence staining of heart sections with Nogo-B (red), endothelial cell marker VE-cadherin (VEC, green) and nuclei DAPI, from ApoE−/−mice after 24-h or (B) 7 weeks TAC. Scale bar: 20 μm. (C–E) Representative Western blotting images and quantifications of protein levels of Nogo-B in whole heart tissues from ApoE−/−and Nogo-A/B−/−ApoE−/−(DKO) mice subject to 24-h (C), or 72-h (D), or 7-week (E) sham and TAC operation. n ≥5 mice/group. P value with statistical significance were labeled above the connected lines between indicated groups (one- way ANOVA with Tukey’s multiple comparisons test). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Frozen heart sections were air dried at room temperature for 10 min, rinsed in PBS, incubated in 0.1% Triton X-100 in 5% BSA solution for 1 h at 37 ◦C, then co-stained overnight in 5% BSA solution at 4 ◦C with addition of antibodies against Nogo-A/B (1:200, cat#ab47085, Abcam), VE-cadherin (1:100, cat#sc-9989, Santa Cruz Biotechnology), αSMA (1:100, cat#67735-1-Ig, Proteintech) or CD68 (1:100, cat#MA513324, Thermo fisher), respectively.

Techniques: Immunofluorescence, Staining, Marker, Western Blot, Labeling