A novel leptin receptor binding peptide tethered-collagen scaffold promotes lung injury repair

归巢(生物学) 间充质干细胞 细胞生物学 再生(生物学) 内生 受体 脚手架 小鼠苗条素受体 瘦素 化学 生物 内分泌学 内科学 生物化学 医学 生物医学工程 肥胖 生态学
作者
Yan Zhuang,Wen Yang,Lulu Zhang,Caixia Fan,Linzi Qiu,Yannan Zhao,Bing Chen,Yanyan Chen,He Shen,Jianwu Dai
出处
期刊:Biomaterials [Elsevier]
卷期号:291: 121884-121884 被引量:3
标识
DOI:10.1016/j.biomaterials.2022.121884
摘要

Lung regeneration after acute injury usually depends on stem cell migration and differentiation, and functional alveoli-like tissue and capillary structure formation. The homing of mesenchymal stem cells (MSCs) to injury sites promotes lung repair through damaged cell replacement and anti-inflammatory and anti-fibrotic effects. Here, we aimed to improve therapeutic effects of the endogenous MSCs by increasing their homing efficiency. We have identified a high-affinity leptin receptor (LEPR)-binding peptide using a phage display screening technique, as the LEPR is highly expressed in MSCs. The selected LEPR-binding peptides were modified with a collagen binding peptide for specifically tethering to a collagen scaffold. After implantation of the LEPR-binding peptide functionalized collagen scaffold in a rat model of acute lung injury, the endogenous LEPR+ MSCs were specifically recruited out of circulation to the scaffold, and their retention periods in the damaged area were significantly prolonged. The migrated MSCs in the functional scaffold promoted the differentiation of type Ⅱ alveolar epithelial cells to type Ⅰ alveolar epithelial cells and facilitated alveoli-like tissue and capillary formation, thus improved lung function recovery. These results suggest that tethering the LEPR binding peptides to the collagen scaffold significantly enhanced endogenous MSC recruitment and promoted functional regeneration of injured lung tissue.
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