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BMP2 和 BMP4 对 VSMC 表型的差异和补偿作用以及 BMP4 在胸主动脉瘤发展中的作用。

Divergent and Compensatory Effects of BMP2 and BMP4 on the VSMC Phenotype and BMP4's Role in Thoracic Aortic Aneurysm Development.

机构信息

Department of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg im Breisgau, Germany.

Institute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, 79104 Freiburg im Breisgau, Germany.

出版信息

Cells. 2024 Apr 24;13(9):735. doi: 10.3390/cells13090735.

DOI:10.3390/cells13090735
PMID:38727271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11083443/
Abstract

Vascular smooth muscle cells (VSMCs) play a key role in aortic aneurysm formation. Bone morphogenetic proteins (BMPs) have been implicated as important regulators of VSMC phenotype, and dysregulation of the BMP pathway has been shown to be associated with vascular diseases. The aim of this study was to investigate for the first time the effects of BMP-4 on the VSMC phenotype and to understand its role in the development of thoracic aortic aneurysms (TAAs). Using the angiotensin II (AngII) osmotic pump model in mice, aortas from mice with VSMC-specific BMP-4 deficiency showed changes similar to AngII-infused aortas, characterised by a loss of contractile markers, increased fibrosis, and activation of matrix metalloproteinase 9. When BMP-4 deficiency was combined with AngII infusion, there was a significantly higher rate of apoptosis and aortic dilatation. In vitro, VSMCs with mRNA silencing of BMP-4 displayed a dedifferentiated phenotype with activated canonical BMP signalling. In contrast, BMP-2-deficient VSMCs exhibited the opposite phenotype. The compensatory regulation between BMP-2 and BMP-4, with BMP-4 promoting the contractile phenotype, appeared to be independent of the canonical signalling pathway. Taken together, these results demonstrate the impact of VSMC-specific BMP-4 deficiency on TAA development.

摘要

血管平滑肌细胞 (VSMCs) 在主动脉瘤形成中起着关键作用。骨形态发生蛋白 (BMPs) 被认为是 VSMC 表型的重要调节因子，BMP 途径的失调与血管疾病有关。本研究旨在首次研究 BMP-4 对 VSMC 表型的影响，并了解其在胸主动脉瘤 (TAA) 发展中的作用。使用血管紧张素 II (AngII) 渗透泵模型在小鼠中，VSMC 特异性 BMP-4 缺乏的小鼠的主动脉显示出与 AngII 输注的主动脉相似的变化，其特征是收缩标志物丢失、纤维化增加和基质金属蛋白酶 9 激活。当 BMP-4 缺乏与 AngII 输注相结合时，凋亡和主动脉扩张的发生率明显更高。在体外，用 BMP-4 mRNA 沉默的 VSMCs 表现出去分化表型，伴有激活的经典 BMP 信号通路。相比之下，BMP-2 缺乏的 VSMCs 表现出相反的表型。BMP-2 和 BMP-4 之间的代偿调节，BMP-4 促进收缩表型，似乎独立于经典信号通路。总之，这些结果表明 VSMC 特异性 BMP-4 缺乏对 TAA 发展的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/cabcaa73f743/cells-13-00735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/8cd10f26c82f/cells-13-00735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/389f9b77400a/cells-13-00735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/a2479f576d68/cells-13-00735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/d4a54668e141/cells-13-00735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/361d6185d8b6/cells-13-00735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/f1114b91408c/cells-13-00735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/cabcaa73f743/cells-13-00735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/8cd10f26c82f/cells-13-00735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/389f9b77400a/cells-13-00735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/a2479f576d68/cells-13-00735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/d4a54668e141/cells-13-00735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/361d6185d8b6/cells-13-00735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/f1114b91408c/cells-13-00735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/674b/11083443/cabcaa73f743/cells-13-00735-g007.jpg

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