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Our hypothesis is that the increased pressure leads to increased mechanical stretch in the aortic valve leaflets, inducing a cascade of responses that ultimately result in local tissue fibrosis and AI. The goal of this study is to investigate the mechanism behind this hypothesis using the methods of tissue engineering. A bioreactor has been built that imparts cyclic stretch and flow to small 3-D constructs of living cells cultured in a silicone membrane.

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The approach is to use this device for in vitro tissue culture of vascular interstitial cells VICs embedded in a collagen gel, which will be subjected to normal and altered stretch and shear representative of the in vivo valve biomechanics. The bioreactor was validated to measure the amount of stretch and shear it can impart to closely replicate in-vivo conditions using PIV technique and ImageJ software.

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Mean longitudinal strain of 0. The cells that underwent cycles of stretch and shear in the bioreactor were screened for formation of myofibroblast using techniques of immunohistochemistry. The marker used was?

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Yhe expression of the myofibroblast phenotype is a feature of valvupathy.