Research Paper Volume 12, Issue 10 pp 9726—9744

NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells

Figure 5. YAP is required for NF2 knockdown-mediated neointima hyperplasia after vascular injury. WT and Nf2-/- mice received injection of shCon, shYap, Ad-Con and Ad-Yap into the injured left common carotid artery via the external carotid artery immediately after injury and then incubated for 30 min. The mice subsequently received intravenous injection of these adenovirus via tail vein at 7, 14, 21 days after injury. (A) The relative protein expression levels of p-YAPSer127 and YAP were determined by immunoblotting in arteries of WT and Nf2-/- mice at day 28 after vascular injury (n=5). (B) Representative H&E staining of carotid arteries from WT or Nf2-/- mice treated as above mentioned (left) and corresponding quantification for ratio of intima/media (right) were shown (n=5). Magnification 200×. (C) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2-/- mice treated as above mentioned (left) and corresponding quantification for Ki-67-positive cells within neointima (right) were shown (n=5). Magnification 200×. Data are shown as mean ± S.D. *P<0.05, **P<0.01 and ***P<0.001 denote statistical comparison between the two marked groups, respectively.