文献类型：期刊文献

英文题名：Sulfated polysaccharide directs therapeutic angiogenesis via endogenous VEGF secretion of macrophages

作者：Yu, Yuanman[1];Dai, Kai[1];Gao, Zehua[2];Tang, Wei[3];Shen, Tong[2];Yuan, Yuan[2];Wang, Jing[1];Liu, Changsheng[2]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]East China Univ Sci & Technol, Key Lab Ultrafine Mat, Minist Educ, Shanghai 200237, Peoples R China;[3]Chinese Acad Sci, Shenzhen Inst Adv Technol, Shenzhen Key Lab Nanobiomech, Shenzhen 518055, Peoples R China

年份：2021

卷号：7

期号：7

外文期刊名：SCIENCE ADVANCES

收录：;EI(收录号：20210709930853);WOS:【SCI-EXPANDED(收录号:WOS:000617708700019)】；

基金：This research was supported by the National Natural Science Foundation of China for Innovative Research Groups (no. 51621002) and the National Natural Science Foundation of China (no. 31870953). This study was also supported by the 111 Project (B14018).

语种：英文

外文关键词：Diseases

摘要：Notwithstanding the remarkable progress in the clinical treatment of ischemic disease, proangiogenic drugs mostly suffer from their abnormal angiogenesis and potential cancer risk, and currently, no off-the-shelf biomaterials can efficiently induce angiogenesis. Here, we reported that a semisynthetic sulfated chitosan (SCS) readily engaged anti-inflammatory macrophages and increased its secretion of endogenous vascular endothelial growth factor (VEGF) to induce angiogenesis in ischemia via a VEGF-VEGFR2 signaling pathway. The depletion of host macrophages abrogated VEGF secretion and vascularization in implants, and the inhibition of VEGF or VEGFR2 signaling also disrupted the macrophage-associated angiogenesis. In addition, in a macrophage-inhibited mouse model, SCS efficiently helped to recover the endogenous levels of VEGF and the number of CD31(hi)Emcn(hi) vessels in ischemia. Thus, both sulfated group and pentasaccharide sequence in SCS played an important role in directing the therapeutic angiogenesis, indicating that this highly bioactive biomaterial can be harnessed to treat ischemic disease.