Small extracellular vesicles as mediators of paracrine senescence in cellular models of aging (IMAGE)
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Figure 1. p16INK4A-expressing IMR-90 release more sEV than proliferating IMR-90 cells. (A) Quantification of CDKN2A mRNA levels by qPCR in IMR-90 fibroblasts expressing a control vector (C), a H-RASG12V vector (RAS) or the ectopic expression of p16INK4A (p16). (B) Heatmap showing the relative mRNA levels related to SASP transcripts in C, RAS and p16 cells by qPCR. The data show the mean from three independent experiments. (C, D) ELISA for (C) IL-6 and (D) IL-1β in the conditioned media of C, RAS and p16 expressing cells. Data show the mean ± SEM of 3 experiments. (E) Representative immunoblot for sEV markers (ALIX, TSG101 and CD9) in sEV isolated from C and p16 IMR-90. 3x109 sEV were loaded per lane. Immunoblot is representative of 3 independent biological replicates. (F) NTA (Nanoparticle Tracking Analyses) measuring the number of sEV released by C, RAS or p16 expressing IMR-90 cells. (G) Flow cytometry histogram and (H) quantification of CD63+/CD81+ sEV released from C and p16 IMR-90 cells captured onto aldehyde/sulphate latex beads. A representative experiment of 3 biological replicates is shown. (I) NTA analyses measuring particle size in sEV isolated from C, RAS and p16 cells. Data represent the mean ± SEM of 3 experiments. Unpaired parametric Student’s t-test was performed. Related to Supplementary Figure 1.
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Copyright: © 2026 Llabrés-Mas et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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