Fig 2: The immunohistochemical staining shows difference between control group and aspirin group (original magnification ×40): platelet-derived growth factor A (PDGF-A) expression on day 1 in the control (A, =moderate) and in the aspirin group (E, =mild), and on day 3 in the control (B, =strong) and in the aspirin group (F, =moderate); platelet-derived growth factor B (PDGF-B) expression on day 3 in the control (C, =strong) and in the aspirin group (G, =moderate); and platelet-derived growth factor receptor alpha (PDGFR-a) expression on day 3 in the control (D, =strong) and in the aspirin group (H, =moderate).

Fig 3: CD226 deficiency in platelets decreased the ribosome and autophagy related protein expression in MK/platelets and human Dami cells. (A) S6 ribosomal protein-expressing ribosome in isolated MKs from BM. Scale bar = 50 µm. (B) Lysates of freshly isolated mice platelets were subjected to western blot with anti-S6 ribosomal, PDGF-A, and PDGF-B antibodies. (C) Double immunofluorescence staining for vWF and Beclin1 in the BM slides from CD226fl/flPF4-Cre and CD226 fl/fl mice. Scale bar = 50 µm. (D) Lysates of freshly isolated mice platelets were subjected to western blot with anti-LC3, Beclin1, and CD226 antibodies. (E) Dami cells infected with lentivirus shCD226 were subjected to western blot with anti-LC3, Beclin 1, and CD226 antibodies.

Fig 4: Sleeping Beauty (SB)-mediated gene transduction into neural progenitor and stem cells (NPC) in the subventricular zone (SVZ). A, Schematic of the transposon vectors used in the study (denoted as GFP, P, NP, PNP). IRES, internal ribosome entry site; PDGFA, platelet-derived growth factor subunit A. B, SB transposase promoted genomic integration of the NP vector into NIH3T3 cells. C, Knockdown efficiency was examined for Nf1 and Trp53 in NIH3T3 cells transduced with the NP vector. Expression levels were normalized by Gapdh. Sdha was used as an internal control. Data represent mean ± SEM (n = 3 samples per group). Student's t test (2-tailed), *P < .05 ***P < .001. D, Schematic of electroporation. DNA solution was injected into the left lateral ventricle. E, GFP expression in the SVZ of the mice electroporated with the GFP vector. The brain was analyzed on day 2 after electroporation. Arrowheads point to GFP+ or DsRed+ cells. F, Expression of fluorescent proteins in the brain parenchyma (8 wk) of the mice electroporated with the GFP, P, NP or PNP vectors and the SB expression vector. G, H&E staining of the regions shown in (F). Serial sections were used for the analysis

Fig 5: TAZ-CAMTA1 drives a proliferative endothelial cell population with a YAP/TAZ target gene signature. (A) Schematic for isolation of lung ECs for scRNA-seq. (B) t-SNE plot of clusters of cells observed from scRNA-seq. (C) t-SNE plots showing expression of various marker genes. Red arrows point to cluster showing positive expression. (D) Volcano plot of 806 differentially expressed genes in TAZ-CAMTA1-induced proliferative subpopulation. Wilcoxon rank sum test, adjusted P-value < 0.05. Genes in red have a log(FC) > 1 and genes in blue have a log(FC) < 1. Some pertinent genes and their corresponding points are marked. (E) t-SNE plots of markers from proliferative subpopulation. (F) Immunostaining validation of differentially expressed genes identified from scRNA-seq analysis. White arrows point to positive staining of Pdgfa, Cryab, or S100a6 in P40 TAZ-CAMTA1iEC but not Ctrl lung vessels. Scale bars, 25 µm. (G) GSEA plot showing normalized enrichment score (NES) of YAP-conserved signature in the proliferative subpopulation, NES = 1.8. P < 0.01, FDR = 0.1. (H) t-SNE plots of canonical YAP/TAZ target genes. Red arrows point to the proliferative cluster showing high expression of these genes.