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白细胞介素-1β 通过 ERK1/2 通路诱导基质金属蛋白酶-3 促进间充质干细胞迁移。

Interleukin-1β-induced matrix metalloproteinase-3 via ERK1/2 pathway to promote mesenchymal stem cell migration.

机构信息

Institute of Anatomy and Cell Biology, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, ROC.

Department of Medical Imaging, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC.

出版信息

PLoS One. 2021 May 21;16(5):e0252163. doi: 10.1371/journal.pone.0252163. eCollection 2021.

Abstract

Human umbilical cord Wharton's jelly derived mesenchymal stem cells (hUCMSCs), a source of cell therapy, have received a great deal of attention due to their homing or migrating ability in response to signals emanating from damaged sites. It has been found that IL-1β possesses the ability to induce the expression of matrix metalloproteinase-3 (MMP-3) in bone marrow MSCs. MMP-3 is involved in cell migration in various types of cells, including glioblastoma, vascular smooth muscle, and adult neural progenitor cells. In this study, we proposed that IL-1β influences hUCMSCs migration involving MMP-3. The expression level of MMP-3 in IL-1β-induced hUCMSCs was verified using cDNA microarray analysis, quantitative real-time PCR, ELISA and Western blot. Wound-healing and trans-well assay were used to investigate the cell migration and invasion ability of IL-1β-treated hUCMSCs. In addition, we pre-treated hUCMSCs with interleukin-1 receptor antagonist, MMP-3 inhibitors (ALX-260-165, UK 356618), or transfected with MMP-3 siRNA to confirm the role of MMP3 in IL-1β-induced cell migration. Our results showed that IL-1β induced MMP-3 expression is related to the migration of hUCMSCs. Moreover, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) inhibitor U0126, p38 inhibitor SB205380, JNK inhibitor SP600125 and Akt inhibitor GSK 690693 decreased IL-1β-induced MMP-3 mRNA and protein expression. The migration and invasion ability analyses showed that these inhibitors attenuated the IL-1β-induced migration and invasion ability of hUCMSCs. In conclusion, we have found that IL-1β induces the expression of MMP-3 through ERK1/2, JNK, p38 MAPK and Akt signaling pathways to enhance the migration of hUCMSCs. These results provide further understanding of the mechanisms in IL-1β-induced hUCMSCs migration to injury sites.

摘要

人脐带华通氏胶间充质干细胞(hUCMSCs)作为细胞治疗的一种来源,由于其具有向受损部位发出的信号归巢或迁移的能力而受到广泛关注。已经发现,IL-1β 具有诱导骨髓间充质干细胞表达基质金属蛋白酶-3(MMP-3)的能力。MMP-3 参与包括神经胶质瘤、血管平滑肌和成人神经祖细胞在内的各种类型细胞的迁移。在这项研究中,我们提出,IL-1β 通过 MMP-3 影响 hUCMSCs 的迁移。使用 cDNA 微阵列分析、定量实时 PCR、ELISA 和 Western blot 验证了 IL-1β 诱导的 hUCMSCs 中 MMP-3 的表达水平。使用划痕愈合和 Trans-well 测定法研究了 IL-1β 处理的 hUCMSCs 的细胞迁移和侵袭能力。此外,我们用白细胞介素-1 受体拮抗剂、MMP-3 抑制剂(ALX-260-165、UK 356618)预处理 hUCMSCs,或用 MMP-3 siRNA 转染,以确认 MMP3 在 IL-1β 诱导的细胞迁移中的作用。我们的结果表明,IL-1β 诱导的 MMP-3 表达与 hUCMSCs 的迁移有关。此外,细胞外信号调节蛋白激酶 1 和 2(ERK1/2)抑制剂 U0126、p38 抑制剂 SB205380、JNK 抑制剂 SP600125 和 Akt 抑制剂 GSK 690693 降低了 IL-1β 诱导的 MMP-3 mRNA 和蛋白表达。迁移和侵袭能力分析表明,这些抑制剂减弱了 IL-1β 诱导的 hUCMSCs 的迁移和侵袭能力。总之,我们发现,IL-1β 通过 ERK1/2、JNK、p38 MAPK 和 Akt 信号通路诱导 MMP-3 的表达,增强 hUCMSCs 的迁移。这些结果为进一步了解 IL-1β 诱导的 hUCMSCs 向损伤部位迁移的机制提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbb1/8139494/bfe83cca56db/pone.0252163.g001.jpg

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