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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
Relevance score: 7.7270274Xiongshan Sun, Shuang Li, Xueqing Gan, Ken Chen, Dachun Yang, Yongjian Yang
Keywords: NF2, YAP, TEAD1, neointima hyperplasia, vascular restenosis
Published in Aging on May 18, 2020
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.
VSMC proliferation and migration in vitro is elevated after NF2 knockdown. (A) The relative protein expression levels of p-NF2Ser518 and NF2 were determined by immunoblotting in VSMC after 0, 24 and 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment (n=5). (B) VSMC isolated from WT or Nf2-/- mice was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue) after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. Representative images (left) and corresponding quantification of Ki-67 positive VSMC (right) were shown (n=5). Magnification 400×. (C) Migration of VSMC isolated from WT and Nf2-/- mice after 24 h of physiological saline or PDGF-BB (30 ng/mL) treatment was measured via wound healing assay. Representative images (upper panel) and corresponding quantification of healing rates (lower panel) were shown (n=5). Magnification 100×. (D) VSMC isolated from WT or Nf2-/- mice after 8 h of physiological saline or PDGF-BB (30 ng/mL) treatment was assessed by transwell assay. Representative images (upper panel) and corresponding quantification of migration cells (lower panel) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. **P<0.01 and ***P<0.001 denote statistical comparison between the two marked groups, respectively.
Enhanced NF2 phosphorylation and subsequent nuclear translocation of YAP following PDGF-BB treatment or injury. (A) Nuclear and cytosolic-enriched fractions were prepared from VSMC, which was treated by PDGF-BB (30 ng/mL) for 48 h. The relative protein expression levels of p-NF2Ser518, NF2 and YAP were determined by immunoblotting (n=5). (B) Nuclear and cytosolic-enriched fractions were prepared from arteries of C57BL/6J mice at day 28 after vascular injury. The relative protein expression levels of p-NF2Ser518, NF2 and YAP were determined by immunoblotting (n=5). Data are shown as mean ± S.D. **P<0.01 and ***P<0.001 denote statistical comparison between the two marked groups, respectively.
NF2 knockdown accelerates PDGF-BB-induced VSMC proliferation and migration in a YAP-dependent manner. VSMC isolated from WT or Nf2-/- mice was transfected by shCon, shYap, Ad-Con and Ad-Yap. Then the VSMC received 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. (A) The relative protein expression levels of p-YAPSer127 and YAP were determined by immunoblotting in VSMC treated as above mentioned (n=5). (B) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. (C) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. 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.
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.
NF2 knockdown causes increased VSMC proliferation and migration induced by PDGF-BB via inducing YAP-TEAD1 interaction. (A) VSMC isolated from WT or Nf2-/- mice after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment was subjected to immunoprecipitation using anti-YAP antibody or control IgG. Inputs and immunocomplexes were analyzed by immunoblotting. VSMC isolated from WT and Nf2-/- mice was transfected with control siRNA, Teadi or Ad-Con, Ad-Yap and then treated by physiological saline or PDGF-BB (30 ng/mL) for 48 h. (B) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. (C) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. 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.
The hypothesis of NF2/YAP/TEAD1 signaling axis in VSMC after PDGF-BB stimuli. PDGF-BB excretion after vascular injury induces nuclear NF2 phosphorylation, thereby causing inactivation of NF2. Decreased active NF2 led to dephosphorylation of YAP and subsequent nuclear translocation of YAP. Increased nuclear YAP binds to TEAD1 and positively regulates relative target gene expression.