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δ-生育三烯酚预处理通过抑制与BACH1相关的铁死亡来提高骨髓间充质干细胞促进伤口愈合的能力。

δ-Tocotrienol preconditioning improves the capability of bone marrow-derived mesenchymal stem cells in promoting wound healing by inhibiting BACH1-related ferroptosis.

作者信息

He Xiao, Wang Dawei, Yi Yi, Tan Yufang, Wu Min, Wang Haiping, Hu Weijie, Chen Hongbo, Zhang Qi, Wu Yiping

机构信息

Department of Plastic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.

出版信息

Cell Death Discov. 2023 Sep 22;9(1):349. doi: 10.1038/s41420-023-01653-1.

DOI:10.1038/s41420-023-01653-1
PMID:37739949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10516898/
Abstract

Wound healing is a complex physiological process for maintaining skin integrity after a wound. Bone marrow-derived mesenchymal stem cells (BMSCs) are excellent cellular candidates for wound healing, which could be enhanced by exogenous stimulation. We aimed to explore the role of δ-Tocotrienol (δ-TT) in BMSC ability of wound healing. Firstly, transcriptome and single-cell analysis were used to explore the genes and pathways related to ferroptosis in wound tissues. In vitro, cell proliferation, migration, and angiogenesis of δ-TT-BMSCs were detected. In addition, qRT-PCR and immunofluorescence (IF) were applied for observing the promoting wound healing ability of δ-TT-BMSC conditioned medium (CM) on NIH-3T3 and PAM-212 cells. The level of ferroptosis was determined by the mitochondrial membrane potential and total/lipid reactive oxygen species (ROS) in the cells and the morphological changes of mitochondria were observed by transmission electron microscope. The BTB and CNC homology 1 (BACH1) expression and activation of the PI3K/AKT signaling pathway were detected by IF and western blot (WB). The effect of δ-TT-BMSCs on wound healing was observed in vivo. The regulatory mechanism of δ-TT-BMSCs on ferroptosis was verified by IHC and IF staining. In vitro, δ-TT-BMSCs declined the level of lipid ROS in NIH-3T3 and PAM-212 cells and enhanced mitochondrial membrane potential. In vivo, δ-TT-BMSCs promoted wound healing in mice by decreasing ferroptosis. In terms of mechanism, δ-TT-BMSCs inhibited the expression of BACH1 and activated PI3K/AKT signaling pathway. This study demonstrated the ability of δ-TT-BMSCs to promote wound healing by inhibiting BACH1-related ferroptosis. In addition, PI3K/AKT signaling pathway was activated by δ-TT-BMSCs and could be involved in wound healing. δ-TT-BMSCs might be a promising strategy for treating wounds.

摘要

伤口愈合是一个在伤口后维持皮肤完整性的复杂生理过程。骨髓间充质干细胞（BMSCs）是伤口愈合的优秀细胞候选者，外源性刺激可增强其作用。我们旨在探讨δ-生育三烯酚（δ-TT）在BMSCs伤口愈合能力中的作用。首先，利用转录组和单细胞分析来探索伤口组织中与铁死亡相关的基因和通路。在体外，检测δ-TT-BMSCs的细胞增殖、迁移和血管生成。此外，应用qRT-PCR和免疫荧光（IF）观察δ-TT-BMSC条件培养基（CM）对NIH-3T3和PAM-212细胞的促进伤口愈合能力。通过细胞线粒体膜电位和总/脂质活性氧（ROS）测定铁死亡水平，并通过透射电子显微镜观察线粒体的形态变化。通过IF和蛋白质免疫印迹（WB）检测BTB和CNC同源物1（BACH1）的表达以及PI3K/AKT信号通路的激活。在体内观察δ-TT-BMSCs对伤口愈合的影响。通过免疫组化（IHC）和IF染色验证δ-TT-BMSCs对铁死亡的调控机制。在体外，δ-TT-BMSCs降低了NIH-3T3和PAM-212细胞中的脂质ROS水平并增强了线粒体膜电位。在体内，δ-TT-BMSCs通过减少铁死亡促进小鼠伤口愈合。在机制方面，δ-TT-BMSCs抑制BACH1的表达并激活PI3K/AKT信号通路。本研究证明了δ-TT-BMSCs通过抑制BACH1相关的铁死亡促进伤口愈合的能力。此外，δ-TT-BMSCs激活了PI3K/AKT信号通路，且该通路可能参与伤口愈合。δ-TT-BMSCs可能是一种有前途的伤口治疗策略。

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