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VAP-PLGA 微球（VAP-PLGA）通过 PI3K/Akt/HIF-1α 通路促进脂肪来源干细胞（ADSCs）诱导的小鼠慢性皮肤溃疡愈合。

VAP-PLGA microspheres (VAP-PLGA) promote adipose-derived stem cells (ADSCs)-induced wound healing in chronic skin ulcers in mice via PI3K/Akt/HIF-1α pathway.

机构信息

First Clinical School Medicine, Nanjing University of Chinese Medicine, Nanjing City, China.

Department of Plastic Surgery, Affiliated Hospital Nanjing University of Chinese Medicine, Nanjing City, China.

出版信息

Bioengineered. 2021 Dec;12(2):10264-10284. doi: 10.1080/21655979.2021.1990193.

DOI:10.1080/21655979.2021.1990193
PMID:34720043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8810082/
Abstract

Chronic skin ulcers are a primary global health problem. Velvet antler polypeptide (VAP) regulates endothelial cell migration and angiogenic sprout. Adipose-derived stem cells (ADSCs) are reported to make pivotal impacts upon wound healing. This study aimed to explore the role of VAP combined with ADSCs in wound healing of chronic skin ulcers. The effect of VAP on phenotypes of ADSCs, and VAP (PLGA microspheres) combining with ADSCs on wound healing of chronic skin ulcers was evaluated. VAP generally promoted the proliferation, migration and invasion of ADSCs, and ADSC-induced angiogenesis in human umbilical vein endothelial cells (HUVECs) through PI3K/Akt/HIF-1α pathway. VAP-PLGA (PLGA microspheres) enhanced the promoting effect of ADSCs on wound healing, pathological changes, and angiogenesis in chronic skin ulcers . VAP-PLGA intensified the effect of ADSCs on up-regulating the levels of p-PI3K/PI3K, p-Akt/Akt, HIF-1α, vascular endothelial growth factor (VEGF), stromal cell-derived factor-1 (SDF-1), C-X-C motif chemokine receptor 4 (CXCR4), angiopoietin-4 (Ang-4), VEGF receptor (VEGFR), and transforming growth factor-β1 (TGF-β1), and down-regulating the levels of interleukin-1 β (IL-1β), IL-18 and IL-6 in wound tissues in chronic skin ulcers . Collectively, VAP promoted the growth, migration, invasion, and angiogenesis of ADSCs through activating PI3K/Akt/HIF-1α pathway, and VAP-PLGA enhanced the function of ADSCs in promoting wound healing , which was associated with angiogenesis, inflammation inhibition, and dermal collagen synthesis.

摘要

慢性皮肤溃疡是一个全球性的主要健康问题。鹿茸多肽（VAP）调节内皮细胞迁移和血管生成芽。脂肪来源的干细胞（ADSCs）被报道对伤口愈合有重要影响。本研究旨在探讨 VAP 联合 ADSCs 在慢性皮肤溃疡愈合中的作用。评估了 VAP 对 ADSCs 表型的影响，以及 VAP（PLGA 微球）与 ADSCs 联合对慢性皮肤溃疡愈合的影响。VAP 通常通过 PI3K/Akt/HIF-1α 通路促进 ADSCs 的增殖、迁移和侵袭，以及 ADSC 诱导人脐静脉内皮细胞（HUVECs）的血管生成。VAP-PLGA（PLGA 微球）增强了 ADSCs 对慢性皮肤溃疡愈合、病理变化和血管生成的促进作用。VAP-PLGA 增强了 ADSCs 上调 p-PI3K/PI3K、p-Akt/Akt、HIF-1α、血管内皮生长因子（VEGF）、基质细胞衍生因子-1（SDF-1）、C-X-C 基序趋化因子受体 4（CXCR4）、血管生成素-4（Ang-4）、血管内皮生长因子受体（VEGFR）和转化生长因子-β1（TGF-β1）水平的作用，并下调慢性皮肤溃疡组织中白细胞介素-1β（IL-1β）、IL-18 和 IL-6 的水平。总之，VAP 通过激活 PI3K/Akt/HIF-1α 通路促进 ADSCs 的生长、迁移、侵袭和血管生成，VAP-PLGA 增强了 ADSCs 促进伤口愈合的功能，这与血管生成、炎症抑制和真皮胶原合成有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4581/8810082/11d5552e6de5/KBIE_A_1990193_F0010_OC.jpg
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