Loss of flow responsive Tie1 results in Impaired Aortic valve remodeling

Qu, Xiaomei; Violette, Kate; Sewell-Loftin, Mary Kathryn; Soslow, Jonathan H.; Saint-Jean, Leshana; Hinton, Robert B.; Merryman, W. David; Baldwin, H. Scott

doi:10.1016/j.ydbio.2019.07.011

Cited by 9 publications

(9 citation statements)

References 40 publications

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“…Tie-1 is upregulated by oscillating shear stress and differentially expressed in a dynamic pattern with disturbed flow [32]. Tie-1 deletion in mice causes abnormal extracellular matrix deposition and remodeling characterized by increased glycosaminoglycan and decreased collagen content.…”

Section: How Do Endothelial Cells Facilitate Repair?mentioning

confidence: 99%

COVID-19-associated vasculitis and vasculopathy

Becker

2020

J Thromb Thrombolysis

246

259

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The COVID-19 pandemic now totaling 13,000,000 cases and over 571,000 deaths has continued to teach the medical, scientific and lay communities about viral infectious disease in the modern era. Among the many lessons learned for the medical community is the potential for transmissibility and host infectivity of the SARS-CoV-2 virus. Moreover, it has become clear that the virus can affect any organ including the circulatory system, directly via either tissue tropism or indirectly stemming from inflammatory responses in the form of innate immunity, leukocyte debris such as cell-free DNA and histones and RNA viral particles. The following review considers COVID-19-associated vasculitis and vasculopathy as a defining feature of a virus-induced systemic disease with acute, subacute and potential chronic health implications.

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Section: How Do Endothelial Cells Facilitate Repair?mentioning

confidence: 99%

COVID-19-associated vasculitis and vasculopathy

Becker

2020

J Thromb Thrombolysis

246

259

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“…Similarly, Notch1 activation is restricted to the VECs on the atrialis/ ventricularis side of developing valve leaflets during elongation (Goddard et al, 2017;MacGrogan et al, 2016). Likewise, loss of the endothelial-specific receptor tyrosine kinase Tie1, which is upregulated by oscillatory shear stress (OSS; see Glossary, Box 1) and is expressed by VECs on the fibrosa side, leads to enlarged aortic valves with increased glycosaminoglycan (GAG) and decreased collagen content (Qu et al, 2019). Thus, flowresponsive signaling pathways are involved in VEC diversification.…”

Section: Valve Endothelial Cell (Vec)mentioning

confidence: 99%

“…Consequently, disruption of downstream mechanosensitive genes has been used to examine biomechanically regulated molecular pathways of valve development. Indeed, this approach has been used to identify many mechanosensitive proteins that are involved in VEC diversification, including KLF2, Notch1 and Tie2 (Goddard et al, 2017;MacGrogan et al, 2016;Qu et al, 2019); however, additional studies are required to identify novel mechanosensitive proteins present in the valve. One avenue for identifying potential biomechanically regulated mechanisms is to study the development of other types of vascular valves, including lymphatic valves, venous valves and lymphovenous valves (Petrova et al, 2004;Bazigou et al, 2011;Geng et al, 2016).…”

Section: The Role Of Blood Flow and Biomechanical Forces In Valve Developmentmentioning

confidence: 99%

Mechanisms of heart valve development and disease

O’Donnell

Yutzey

2020

Development

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The valves of the heart are crucial for ensuring that blood flows in one direction from the heart, through the lungs and back to the rest of the body. Heart valve development is regulated by complex interactions between different cardiac cell types and is subject to blood flow-driven forces. Recent work has begun to elucidate the important roles of developmental pathways, valve cell heterogeneity and hemodynamics in determining the structure and function of developing valves. Furthermore, this work has revealed that many key genetic pathways involved in cardiac valve development are also implicated in diseased valves. Here, we review recent discoveries that have furthered our understanding of the molecular, cellular and mechanosensitive mechanisms of valve development, and highlight new insights into congenital and acquired valve disease.

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“…To compensate for stenotic conditions, the change in hemodynamics due to stenosis can also lead to left ventricular remodeling (106). For instance, gene expression of Tie1 in valvular endothelial cells may be essential for ECM remodeling in valve tissues (107), as Tie1 is found to be necessary for endothelial cell proliferation (108). However, due to its orphan receptor status, Tie1 is still poorly characterized (109).…”

Section: Biomechanical Contextmentioning

confidence: 99%

Oscillatory fluid-induced mechanobiology in heart valves with parallels to the vasculature

2020

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Forces generated by blood flow are known to contribute to cardiovascular development and remodeling. These hemodynamic forces induce molecular signals that are communicated from the endothelium to various cell types. The cardiovascular system consists of the heart and the vasculature, and together they deliver nutrients throughout the body. While heart valves and blood vessels experience different environmental forces and differ in morphology as well as cell types, they both can undergo pathological remodeling and become susceptible to calcification. In addition, while the plaque morphology is similar in valvular and vascular diseases, therapeutic targets available for the latter condition are not effective in the management of heart valve calcification. Therefore, research in valvular and vascular pathologies and treatments have largely remained independent. Nonetheless, understanding the similarities and differences in development, calcific/fibrous pathologies and healthy remodeling events between the valvular and vascular systems can help us better identify future treatments for both types of tissues, particularly for heart valve pathologies which have been understudied in comparison to arterial diseases.

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Loss of flow responsive Tie1 results in Impaired Aortic valve remodeling

Cited by 9 publications

References 40 publications

COVID-19-associated vasculitis and vasculopathy

COVID-19-associated vasculitis and vasculopathy

Mechanisms of heart valve development and disease

Oscillatory fluid-induced mechanobiology in heart valves with parallels to the vasculature

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Loss of flow responsive Tie1 results in Impaired Aortic valve remodeling

Cited by 9 publications

References 40 publications

COVID-19-associated vasculitis and vasculopathy

COVID-19-associated vasculitis and vasculopathy

Mechanisms of heart valve development and disease

Oscillatory fluid-induced mechanobiology in heart valves with parallels to the vasculature

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Product

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Loss of flow responsive Tie1 results in Impaired Aortic valve remodeling