IL-1β promotes A7r5 and HASMC migration and invasion via the p38-MAPK/Angpt-2 pathway.
IL-1β promotes A7r5 and HASMC migration and invasion via the p38-MAPK/Angpt-2 pathway.
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DOI：
10.1186/s40001-022-00781-1
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发表时间：
2022-08-17
影响因子：
4.2
通讯作者：
Wang, Jing
中科院分区：
文献类型：
--
作者：
Xu, Anyu;Pei, Jingchun;Yang, Yunhong;Hua, Baotong;Wang, Jing
血管平滑肌细胞（vascular smooth muscle cell，VSMCs）的迁移、增殖和炎症因子的分泌参与了包括冠状动脉粥样硬化（coronary atherosclerosis，CAS）在内的多种血管闭塞性疾病的重要病理过程。白细胞介素1 β（IL-1 β）作为VSMC合成和分泌的生物活性介质，可促进CAS的病理进展。本研究进一步探讨了IL-1 β调控VSMC迁移、侵袭的分子机制。用IL-1 β预处理A7r5和HASMC 24 h，Western blotting法检测细胞中IL-1 β、增殖细胞核抗原（PCNA）、细胞周期蛋白D1（cyclin D1）、基质金属蛋白酶2（MMP 2）和基质金属蛋白酶9（MMP 9）的表达。细胞迁移和侵袭能力通过Transwell和伤口愈合测定来测量。通过MTT测定测量细胞活力。IL-1 β可上调A7r5和HASMC增殖相关蛋白（PCNA和Cyclin D1）的表达，诱导MMP 2和MMP 9的分泌，促进细胞侵袭和迁移。此外，IL-1 β处理A7r5和HASMCs后，Angpt-2表达呈时间依赖性增加，si-Angpt-2转染抑制细胞迁移和侵袭，MMP 2和MMP 9表达下调。同时，我们进一步发现IL-1 β诱导的细胞中p38-MAPK通路被激活，p38-MAPK抑制剂可下调Angpt-2的表达。总之，这些数据表明IL-1 β通过p38-MAPK/Angpt-2途径促进A7r5和HASMC迁移和侵袭。
The migration, proliferation, and inflammatory factor secretion of vascular smooth muscle cells (VSMCs) are involved in the important pathological processes of several vascular occlusive diseases, including coronary atherosclerosis (CAS). Interleukin 1β(IL-1β), as a bioactive mediator of VSMC synthesis and secretion, can promote the pathological progress of CAS. In this study, we further explored the underlying molecular mechanisms by which IL-1β regulates VSMC migration, invasion. We pretreated A7r5 and HASMC with IL-1β for 24 h, and measured the expression of IL-1β, proliferating cell nuclear antigen (PCNA), cyclin D1, matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 2 (MMP9) in the cells by Western blotting. Cell migration and invasion ability were measured by Transwell and wound healing assays. Cell viability was measured by an MTT assay. We found that IL-1β upregulated the expression of proliferation-related proteins (PCNA and Cyclin D1) in A7r5 and HASMC, and induces the secretion of MMP2 and MMP9, promotes cell invasion and migration. In addition, in A7r5 and HASMCs treated with IL-1β, the expression of Angiopoietin-2 (Angpt-2) increased in a time-dependent manner, transfection with si-Angpt-2 suppressed cell migration and invasion, with downregulated MMP2 and MMP9 expression. Parallelly, we further found that the p38-MAPK pathway is activated in cells induced by IL-1β, p38-MAPK inhibitors can down-regulate the expression of Angpt-2. Collectively, these data demonstrated that IL-1β promotes A7r5 and HASMC migration and invasion via the p38-MAPK/Angpt-2 pathway.
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