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Hypoxia preconditioned DPSC-derived exosomes regulate angiogenesis via transferring LOXL2
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Zhou, Yanling
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Sun Yat Sen Univ, Hosp Stomatol, Guangzhou 510055, Peoples R China
Guangdong Prov Key Lab Stomatol, Guangzhou 510080, Peoples R China
Sun Yat Sen Univ, Guanghua Sch Stomatol, Guangzhou 510055, Peoples R China Sun Yat Sen Univ, Hosp Stomatol, Guangzhou 510055, Peoples R China

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Liao, Chenxi
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Sun Yat Sen Univ, Hosp Stomatol, Guangzhou 510055, Peoples R China
Guangdong Prov Key Lab Stomatol, Guangzhou 510080, Peoples R China
Sun Yat Sen Univ, Guanghua Sch Stomatol, Guangzhou 510055, Peoples R China Sun Yat Sen Univ, Hosp Stomatol, Guangzhou 510055, Peoples R China

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[1] Sun Yat Sen Univ, Hosp Stomatol, Guangzhou 510055, Peoples R China
[2] Guangdong Prov Key Lab Stomatol, Guangzhou 510080, Peoples R China
[3] Sun Yat Sen Univ, Guanghua Sch Stomatol, Guangzhou 510055, Peoples R China
关键词:
Hypoxia;
Dental pulp stem cells;
Exosomes;
Angiogenesis;
Proteomics;
Lysyl oxidase-like 2;
CROSS-LINKING;
STEM-CELLS;
LYSYL;
NICHE;
D O I:
10.1016/j.yexcr.2023.113543
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 [肿瘤学];
摘要:
Hypoxia was proved to enhance the angiogenesis of stem cells. However, the mechanism of the angiogenic potential in hypoxia-pretreated dental pulp stem cells (DPSCs) is poorly understood. We previously confirmed that hypoxia enhances the angiogenic potential of DPSC-derived exosomes with upregulation of lysyl oxidase-like 2 (LOXL2). Therefore, our study aimed to illuminate whether these exosomes promote angiogenesis via transfer of LOXL2. Exosomes were generated from hypoxia-pretreated DPSCs (Hypo-Exos) stably silencing LOXL2 after lentiviral transfection and characterized with transmission electron microscopy, nanosight and Western blot. The efficiency of silencing was verified using quantitative real-time PCR (qRT-PCR) and Western blot. CCK-8, scratch and transwell assays were conducted to explore the effects of LOXL2 silencing on DPSCs proliferation and migration. Human umbilical vein endothelial cells (HUVECs) were co-incubated with exosomes to assess the migration and angiogenic capacity through transwell and matrigel tube formation assays. The relative expression of angiogenesis-associated genes was characterized by qRT-PCR and Western blot. LOXL2 was successfully silenced in DPSCs and inhibited DPSC proliferation and migration. LOXL2 silencing in Hypo-Exos partially reduced promotion of HUVEC migration and tube formation and inhibited the expression of angiogenesis-associated genes. Thus, LOXL2 is one of various factors mediating the angiogenic effects of Hypo-Exos.
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