Creation and Analysis of Vascular Smooth Muscle Cell Lines Isolated from a Patient with a Bicuspid Aortic Valve

Maria Rodríguez^*
*Correspondence: Maria Rodríguez, Department of Thoracic Vascular Surgery, Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168 Rome, Italy, Email:

Introduction

The Vascular Smooth Muscle Cells (VSMCs) play a pivotal role in the structure and function of the vascular system. They are integral in maintaining vascular tone, regulating blood pressure and contributing to vascular remodeling in response to injury or disease. Vascular smooth muscle dysfunction has been implicated in a variety of cardiovascular diseases, including hypertension, atherosclerosis and aneurysms. In the context of congenital heart diseases, the Bicuspid Aortic Valve (BAV) represents one of the most common structural abnormalities, affecting approximately 1-2% of the population. BAV is associated with an increased risk of developing aortic aneurysms and other vascular complications. Understanding the molecular and cellular mechanisms underlying these vascular abnormalities is essential for the development of targeted therapeutic strategies. However, the mechanisms linking BAV to vascular pathology remain poorly understood due to the lack of appropriate experimental models. While animal models and human tissue samples have provided some insights, there is a significant need for cell-based models that can capture the specific characteristics of vascular smooth muscle cells in BAV patients [1].

This study aims to generate and characterize Vascular Smooth Muscle Cell (VSMC) lines derived from a patient with a bicuspid aortic valve. By establishing these cell lines, we seek to better understand the cellular and molecular underpinnings of vascular dysfunction associated with BAV. The establishment of these patient-specific cell lines provides a novel approach for studying vascular smooth muscle behavior in the context of BAV-related disease and potentially for developing new therapeutic strategies to mitigate the associated risks [2].

Description

Bicuspid aortic valve disease is often considered a silent condition, with many patients remaining asymptomatic for years. However, as the condition progresses, it can lead to the development of serious cardiovascular issues such as aortic dilation, aortic aneurysms and aortic dissection, all of which are associated with high mortality rates if left untreated. The underlying pathophysiology of these complications has been linked to structural and functional abnormalities in the aortic wall, particularly in the vascular smooth muscle cells that comprise the aortic media. These cells are responsible for maintaining the elasticity and mechanical strength of the aorta and their dysfunction can result in the maladaptive remodeling of the vessel wall [3].

BAV is thought to alter the hemodynamic environment of the aorta, causing abnormal blood flow patterns that can place excessive mechanical stress on the vessel wall, especially in the ascending aorta. This altered flow may lead to structural changes in the aortic wall, including the remodeling of extracellular matrix components and changes in the phenotype of vascular smooth muscle cells. VSMCs in the aorta may undergo a phenotypic switch, from a contractile phenotype to a synthetic phenotype, which is associated with increased proliferation, migration and extracellular matrix production. These processes are thought to contribute to the progressive dilation and weakening of the aortic wall [4].

Understanding the mechanisms driving these changes in VSMCs is critical for developing targeted therapies for BAV-related aortic disease. While animal models have provided some insights, human-specific cell-based models offer a more accurate representation of the disease. Patient-derived cell lines can be used to investigate the molecular alterations specific to BAV and to evaluate potential treatments in a way that reflects human disease biology. Therefore, the goal of this study was to generate immortalized VSMC lines from a patient with BAV, which would serve as a valuable tool for studying the cellular and molecular mechanisms underlying BAV-associated vascular disease [5].

Conclusion

The generation and characterization of vascular smooth muscle cell lines derived from a patient with bicuspid aortic valve disease have provided valuable insights into the cellular and molecular mechanisms underlying BAVrelated vascular pathology. By creating a patient-specific model, this study has identified several key differences in the phenotype, gene expression and functional responses of VSMCs derived from BAV patients compared to those from healthy controls. These findings suggest that altered VSMC behavior, including increased proliferation, migration and resistance to apoptosis, may play a critical role in the vascular remodeling and aortic dilation seen in BAV.

Acknowledgement

None.

Conflict of Interest

None.

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