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P16
Layer-Specific Changes in Collagen Fiber Architecture in Calcific Aortic Valve Disease

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Layer-Specific Changes in Collagen Fiber Architecture in Calcific Aortic Valve Disease

Introduction

Extracellular matrix (ECM) “disarray” is a hallmark of calcific aortic valve disease (CAVD). As ECM is known to be a powerful regulator of valvular interstitial cell function, a thorough understanding of ECM “disarray” in CAVD would provide valuable insight into alterations in cellular function. Existing in vitro studies and analyses of native valve tissues have focused almost exclusively on bulk changes in ECM composition, with little attention paid to the nano- and micro- scale architecture where cells directly interact with these structures. In other cell types, fiber organization has been shown to regulate behaviors such as cell polarity, motility, proliferation, and differentiation. Therefore, it is possible that changes in ECM microstructure occurring during CAVD are influencing both biological and mechanical functions of the valve. Second harmonic generation microscopy (SHG) allows for quantification of fibrillar collagen, a major component of the aortic valve architecture, without the use of exogenous treatments.  In this study, traditional histology techniques were used together with SHG to characterize the microstructural remodeling of fibrillar collagen in CAVD and investigate potential causes for these architectural changes.


Conclusions
 
Previous studies of valves with CAVD have noted an increase in collagen disorganization, but the nature of this “disorganization” has not been clearly described, nor have its causes been elucidated. In the current work, we demonstrate differences in the amount, architecture, and post-translational modification of collagen in diseased aortic valves. To our knowledge, this is the first study to examine fiber-level alterations in collagen architecture in human tissues with CAVD. The responsiveness of many other cell types to changes in nano/micro-topographies motivates future investigations into whether these changes in ECM architecture are capable of influencing VIC function and/or calcification. The implications for this work range from gaining insight into the biological and mechanical events in valve pathology to informing the creation of scaffold environments for tissue engineering of valves.
 


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