Phospho-Caveolin 1 (Tyr14) Antibody - #AF3386

EPG inhibited apoptosis and decreased STIM via p-caveolin-1 against MI injury in myocardium of rats (n = 4-6/group). (A) TUNEL staining, apoptotic nuclei (green) and DAPI-positive normal nuclei (blue). (B) Immuno-histochemical staining of p-caveolin-1 and STIM1. (C) Apoptotic rate (%). (D, E) Quantitative mean fluorescence intensity (MFI). ###P < 0.001 vs. sham, ∗∗∗P < 0.001 vs. model, & P < 0.05, &&&P < 0.001 vs. EPG.

Fig. 5 P-Caveolin-1/SOCE pathway mediated EPG-induced protection against MI injury in rats (n = 4-6/group). (A) Western blot bands. Quantitative analysis of protein expression (B–F) and mRNA expression (G-J).

Figure 5: Cav-1 inhibits migration and proliferation of BMECs through suppressing EGFR/AKT/PI3K signaling. (A) BMECs were cultured and treated with different dose of erlotinib (0, 5, 10 µM). Scratch wound healing assay was performed to observe the effect of erlotinib on the migration of BMECs. Scale bar, 100 µm. (B) Quantitative analysis of wound healing rate. (C) Representative images of immunofluorescence staining for Ki67 (green) in BMECs treated with different dose of erlotinib (0, 10 µM). Nuclei were stained with DAPI (blue). White arrows indicate Ki67+ cells. Scale bar, 100 µm. (D) Quantification of the percentage of Ki67+ nuclei among the total nuclei. (E) Representative western blot images for p-AKT, AKT, p-Cav-1, Cav-1, PI3K, and p-PI3K in the BMECs treated with 10 µM erlotinib and GAPDH was used as reference proteins for data normalization. (F) The phosphorylation levels of AKT, Cav-1, PI3K protein were quantified and normalized to their total proteins respectively. (G) Representative images of double immunofluorescence staining for Ki67/EMCN. White arrows indicate Ki67+/EMCN+ cells. Scale bar, 50 µm. (H) Quantitative analysis of Ki67+/EMCN+ cells respectively per area of trabecular bone surface. Data were presented as mean ± SE. *p < 0.05 and **p < 0.01 as determined by one-way ANOVA or two-tailed unpaired t-test.