Skip to main content
. 2022 Nov 9;8(45):eabn6579. doi: 10.1126/sciadv.abn6579

Fig. 2. Vascular ECs undergo apoptosis in response to in vivo cytotoxic treatment and express high levels of proapoptotic BCL-2 family member genes.

Fig. 2.

(A to D) Representative images of immunofluorescence staining for CD31 and Cl-Casp3 in (A) liver, (B) kidney, (C) heart, and (D) lung from P70 mice 12 hours after either sham treatment or 24-Gy whole-body γ-irradiation. Filled arrowheads indicate examples of cells that are positive for both CD31 and Cl-Casp3; empty arrowheads indicate cells that are positive for only Cl-Casp3. n = 3 animals per treatment condition. (E to H) Quantification of number of Cl-Casp3+ cells in CD31+ or CD31− cells per 20× field of view from immunofluorescence images of sham or 24 Gy–irradiated (E) liver, (F) kidney, (G) heart, and (H) lung. n = 15 (3 animals per treatment condition, 5 images per animal). (I and J) Single-cell RNA-seq data for genes involved in mitochondrial apoptosis in ECs, VSMCs, and parenchymal cells of adult mouse heart, liver, lung, and kidney. Expression data mined from (I) the Tabula Muris database (20) and (J) Hupe et al. (22).