CD63 Antibody - #DF2305

Fig. 1 Effect of MSCs-Exo-IDO on renal functions in IRI mouse model. A The protein content of IDO in MSCs-Exo-NC or MSCs-Exo-IDO was firstly detected by Western Blot (n = 3). B Quantization diagram of panel A as shown in the right. Then, IRI mouse model was established. IRI mice were challenged with MSCs-Exo-NC or MSCs-Exo-IDO. Next, serum was obtained from different group mice on days 0, 1, 3 and 7 after IRI. BUN C and Scr D contents were detected by the corresponding ELISA kits (n = 3/group, the results for the same mice at each time). E Kidney tissues were collected from the four groups on day 1, 3 and 7 after IRI (n = 3/group at each time). Kidney tissues in different groups were obtained and histopathology was monitored by HE staining. Arrowheads indicated the damaged tubular. The line chart is presented by Means ± SD, and the statistical analysis was performed using one-way ANOVA. **P 

Fig. 5. Effects of ADSCs-Exo with abundant HOXB3OS on HG-induced podocyte damage. (A) HOXB3OS levels in ADSCs 72 h after transfection with control or HOXB3OS overexpressing plasmid. (B-E) After transfection of control plasmid or HOXB3OS overexpressing plasmid, ADSCsNC-Exo and ADSCsHOXB3OS-Exo were obtained. (B) CD9, CD63, and CD81 protein levels in exosomes. (C) Exosome particle size distribution. (D) Exosome protein concentrations. (E) HOXB3OS levels in exosomes. (F-I) MPC5 cells were treated with NG or HG stimulation for 72 h, and simultaneously treated with 6.25–50 μg/mL ADSCsNC-Exo or ADSCsHOXB3OS-Exo, respectively. (F) HOXB3OS levels in MPC5 cells. (G) SIRT1 protein levels in MPC5 cells, with quantification shown on the right. (H) Cell viability. (I) Apoptosis levels, with quantification shown on the left. Data were expressed as Mean±SD. ** denotes p 

Figure 2. | Identification of EVs derived from LPS-stimulated DPCs (LPS-EVs) and establishment of in vitro model.(g) Western blot analysis of EVs surface markers (CD9, CD63, CD81 and TSG101).

Figure 1. Higher expression of EV surface marker CD63 in apical papilla of rat apical periodontitis model. (b and c) Apical papilla from healthy and inflamed mandibular incisors (n=3) was examined using immunohistochemical staining. Expression of CD63 (EV surface marker), caspase-3, and tumor necrosis factor-a (TNF-a) could barely be detected within healthy apical papilla (left). Significant upregulation of CD63, caspase-3, and TNFa were observed in inflamed apical papilla (right).

Fig. 2. Lovastatin increased IDE-enriched exosome secretion in sevoflurane-exposed BV-2 cells. (A) The mRNA level of IDE in BV-2 cells analyzed by Realtime PCR. (B) CD63 expression detected by flow cytometry. (C) IDE protein level in BV-2 cellderived exosomes. (D) Co-expression of CD63 and IDE examined using immunofluorescence staining. Scale bar: 50 μm. Data were presented as mean ± standard deviation (SD) (N = 3). Significance *P < 0.05, **P < 0.01, and ***P < 0.001. Abbreviations: Control, Con; Sevoflurane, Sevo; Lovastatin, Lova; Sevoflurane + Lovastatin, Sevo + Lova; IDE; Insulin-degrading enzyme.

Figure 1. |Extraction of exosomes from fibroblasts and RSC96 cells. (A) Transmission electron microscopy images of exosomes (yellow arrows) extracted from fibroblasts or RSC96 Schwann cells (magnification, x25,000). Scale bar, 200 nm. (B) Protein expression of exosome marker proteins CD81 and CD63, and the endoplasmic reticulum marker Calnexin were assessed by western blotting.