Journal
SCIENCE ADVANCES
Volume 9, Issue 29, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.adf7858
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Calcification of autologous pathological vessels and tissue engineering blood vessels is a significant clinical challenge. Gli1(+) cells play a role in vascular calcification, and an anticalcification approach utilizing exosomes derived from mesenchymal stem cells delivering lncRNA-ANCR was developed. This approach effectively targeted Gli1(+) cells, inhibited their differentiation into osteoblast-like cells, and prevented vascular calcification.
Calcification of autologous pathological vessels and tissue engineering blood vessels (TEBVs) is a thorny problem in clinic. However, there is no effective and noninvasive treatment that is available against the calcification of TEBVs and autologous pathological vessels. Gli1(+) cells are progenitors of smooth muscle cells (SMCs) and can differentiate into osteoblast-like cells, leading to vascular calcification. Our results showed that the spatiotemporal distribution of Gli1(+) cells in TEBVs was positively correlated with the degree of TEBV calcification. An anticalcification approach was designed consisting of exosomes derived from mesenchymal stem cells delivering lncRNA-ANCR to construct the engineered exosome-Ancr/E7-EXO. The results showed that Ancr/E7-EXO effectively targeted Gli1(+) cells, promoting rapid SMC reconstruction and markedly inhibiting Gli1(+) cell differentiation into osteoblast-like cells. Moreover, Ancr/E7-EXO significantly inhibited vascular calcification caused by chronic kidney disease. Therefore, Ancr/E7-EXO reprogrammed Gli1(+) cells to prevent calcification of vascular graft and autologous pathological vessel, providing unique insights for an effective anticalcification.
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