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 1. NF2 knockdown enhances neointima hyperplasia after vascular injury. WT or Nf2-/- mice received sham operation or wire injury in common carotid artery. (A) The relative protein levels of p-NF2Ser518 and NF2 in common carotid arteries from C57BL/6J mice at day 7, 14 and 28 after injury were analyzed by immunoblotting (n=5). (B) The relative mRNA (n=5) level of Nf2 in common carotid arteries from WT or Nf2-/- mice. (C) The relative protein (n=3) levels of p-NF2Ser518 and NF2 in common carotid arteries from WT or Nf2-/- mice. (D) Representative H&E staining of carotid arteries from WT or Nf2-/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for ratio of intima/media (right) were shown (n=6). Magnification 200×. (E) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2-/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for Ki-67 positive cells within neointima (right) were shown (n=6). 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.