S100B is required for maintaining an intermediate state with double-positive Sca-1+ progenitor and vascular smooth muscle cells during neointimal formation.

Yan WuXin LiuLing-Yun GuoLei ZhangFei ZhengShan LiXing-Yuan LiYe YuanYu LiuYu-Wen YanShi-You ChenJia-Ning WangJin-Xuan ZhangJun-Ming Tang

Published in: Stem cell research & therapy (2019)

S100B triggered neointimal formation in rat injured arteries by maintaining the intermediate state of double-positive Sca-1+ progenitor and VSMCs, which were associated with direct activation of RAGE by S100B and indirect induction of SDF-1α by activating PI3K/AKT and NF-κB.

Keyphrases

vascular smooth muscle cells
pi k akt
signaling pathway
angiotensin ii
cell cycle arrest
cell proliferation
oxidative stress
cell fate
lps induced
inflammatory response
nuclear factor