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Specific Overexpression of YAP in Vascular Smooth Muscle Attenuated Abdominal Aortic Aneurysm Formation by Activating Elastic Fiber Assembly via LTBP4

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Abstract

Abdominal aortic aneurysm (AAA) is a fatal vascular disease. Vascular smooth muscle cells (VSMCs) play a crucial role in the pathogenesis of AAA. Increasing evidence has shown that Yes-associated protein (YAP) is involved in diverse vascular diseases. However, the role of YAP in AAA remains unclear. The current study aimed to determine the role of YAP in AAA formation and the underlying mechanism. We found that YAP expression in VSMCs was markedly decreased in human and experimental AAA samples. Furthermore, VSMC-specific YAP overexpression prevented several pathogenic factor–induced AAA. Mechanistically, YAP overexpression in VSMCs promoted latent transforming growth factor-β binding protein 4 (LTBP4) expression, an important factor in elastic fiber assembly. Finally, silencing of LTBP4 in VSMCs abolished the protective role of YAP in AAA formation in vivo. Our results suggest that YAP promotes LTBP4-mediated elastic fibril assembly in VSMCs, which mitigates elastin degradation and AAA formation.

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Abbreviations

AAA:

Abdominal aortic aneurysm

ANOVA:

Analysis of variance

ECM:

Extracellular matrix

EVG:

Elastica van Gieson

H&E:

Hematoxylin and eosin

HVSMCs:

Human vascular smooth muscle cell

LTBP4:

Latent transforming growth factor-β binding protein 4

PBS:

Phosphate-buffered saline

SMC:

Smooth muscle cell

TGF-β:

Transforming growth factor-β

VSMC:

Vascular smooth muscle cell

YAP:

Yes-associated protein

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Acknowledgements

We thank Dr. Yi Fu for his excellent technical assistance.

Funding

This work was supported by the National Natural Science Foundation of China Grants (81970392, 82070305, 82100268), Beijing Natural Science Foundation of China (J190010), and Tianjin Natural Science Foundation of China (19JCQNJC10100).

Author information

Author notes

  1. Ya-nan Liu and Xue Lv contributed equally to this work and share the first authorship.

Authors and Affiliations

  1. Tianjin Key Laboratory of Metabolic Diseases, Key Laboratory of Immune; The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Medical University, Tianjin, 300070, China

    Ya-nan Liu, Xin Chen & Liu Yao

  2. State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China

    Xue Lv

  3. Department of Pathology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China

    Meng Yan & Ling-chuan Guo

  4. Department of Cardiology, The First Hospital of Hebei Medical University, 89 Donggang Road, Shijiazhuang, 050031, Hebei Province, People’s Republic of China

    Gang Liu

  5. Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education, Beijing Collaborative Innovation Center for Cardiovascular Disorders, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, China

    Hong-feng Jiang

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  1. Ya-nan Liu
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Contributions

Conceived and designed the experiments: Gang Liu, Liu Yao, and Hong-feng Jiang. Material contribution: Meng Yan. Data collection and analysis were performed by Ya-nan Liu, Xue Lv, and Xin Chen. The first draft of the manuscript was written by Ya-nan Liu, Liu Yao, and Hong-feng Jiang. All authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Gang Liu, Liu Yao or Hong-feng Jiang.

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Ethics Statement

The animal study was reviewed and approved by the Committee of Tianjin Medical University on Animal Experimentation (TMUaMEC2021014). All protocols were approved by the First Affiliated Hospital of Soochow University Ethics Committee.

Statement of the Clinical Relevance

AAA is highly lethal disease in humans. This study suggests that early boosting of YAP-LTBP4 pathway in patients with AAA might be an effective strategy to protect against lethality by reducing the risk of aneurysm rupture.

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The authors declare no competing interests.

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Associate Editor Junjie Xiao oversaw the review of this article .

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Liu, Yn., Lv, X., Chen, X. et al. Specific Overexpression of YAP in Vascular Smooth Muscle Attenuated Abdominal Aortic Aneurysm Formation by Activating Elastic Fiber Assembly via LTBP4. J. of Cardiovasc. Trans. Res. 16, 65–76 (2023). https://doi.org/10.1007/s12265-022-10278-1

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