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PIEZO1 通过增强模拟微重力下 CXCR4 的表达促进内皮细胞迁移。

PIEZO1 Promotes the Migration of Endothelial Cells via Enhancing CXCR4 Expression under Simulated Microgravity.

机构信息

Department of Aerospace Medical Training, School of Aerospace Medicine, Air Force Medical University, Xi'an 710032, China.

出版信息

Int J Mol Sci. 2024 Jul 1;25(13):7254. doi: 10.3390/ijms25137254.

DOI:10.3390/ijms25137254
PMID:39000362
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11242226/
Abstract

Exposure to microgravity during spaceflight induces the alterations in endothelial cell function associated with post-flight cardiovascular deconditioning. PIEZO1 is a major mechanosensitive ion channel that regulates endothelial cell function. In this study, we used a two-dimensional clinostat to investigate the expression of PIEZO1 and its regulatory mechanism on human umbilical vein endothelial cells (HUVECs) under simulated microgravity. Utilizing quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis, we observed that PIEZO1 expression was significantly increased in response to simulated microgravity. Moreover, we found microgravity promoted endothelial cells migration by increasing expression of PIEZO1. Proteomics analysis highlighted the importance of C-X-C chemokine receptor type 4(CXCR4) as a main target molecule of PIEZO1 in HUVECs. CXCR4 protein level was increased with simulated microgravity and decreased with PIEZO1 knock down. The mechanistic study showed that PIEZO1 enhances CXCR4 expression via Ca influx. In addition, CXCR4 could promote endothelial cell migration under simulated microgravity. Taken together, these results suggest that the upregulation of PIEZO1 in response to simulated microgravity regulates endothelial cell migration due to enhancing CXCR4 expression via Ca influx.

摘要

在太空飞行期间暴露于微重力会引起与飞行后心血管功能不全相关的内皮细胞功能改变。PIEZO1 是一种主要的机械敏感离子通道，调节内皮细胞功能。在这项研究中，我们使用二维回转仪研究了在模拟微重力下 PIEZO1 在人脐静脉内皮细胞（HUVEC）中的表达及其调节机制。利用定量实时聚合酶链反应（qRT-PCR）和 Western blot 分析，我们观察到 PIEZO1 的表达在模拟微重力下显著增加。此外，我们发现微重力通过增加 PIEZO1 的表达促进内皮细胞迁移。蛋白质组学分析强调了 C-X-C 趋化因子受体 4（CXCR4）作为 PIEZO1 在 HUVEC 中的主要靶分子的重要性。模拟微重力下 CXCR4 蛋白水平增加，而 PIEZO1 敲低则降低。机制研究表明，PIEZO1 通过 Ca 内流增强 CXCR4 的表达。此外，CXCR4 可在模拟微重力下促进内皮细胞迁移。总之，这些结果表明，模拟微重力引起的 PIEZO1 上调通过 Ca 内流增强 CXCR4 的表达来调节内皮细胞迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/affc1cd61ed8/ijms-25-07254-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/3741f68e83a8/ijms-25-07254-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/44ffa991d818/ijms-25-07254-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/a113f5c8bbf3/ijms-25-07254-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/3bf5b93b7533/ijms-25-07254-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/c9220f273c85/ijms-25-07254-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/affc1cd61ed8/ijms-25-07254-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/3741f68e83a8/ijms-25-07254-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/44ffa991d818/ijms-25-07254-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/a113f5c8bbf3/ijms-25-07254-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/3bf5b93b7533/ijms-25-07254-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/c9220f273c85/ijms-25-07254-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/11242226/affc1cd61ed8/ijms-25-07254-g006.jpg

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The Critical Role of The Piezo1/β-catenin/ATF4 Axis on The Stemness of Gli1 BMSCs During Simulated Microgravity-Induced Bone Loss.
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The modes of angiogenesis: an updated perspective.血管生成的模式：一个更新的视角。
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