Calcific aortic valve disease (CAVD) is characterized by the stiffening and calcification of the aortic valve leaflets which result in impaired valve function and increased load on the myocardium. In vitro models of CAVD involve the formation the calcific nodules via aortic valve interstitial cells (AVICs). Transforming growth factor β1 (TGF-β1) induced myofibroblast differentiation of AVICs, which is evidenced by increased αSMA expression, has been shown to be a key mediator of dystrophic calcific nodule formation. Benton et al. demonstrated the critical role of αSMA in nodule formation in that when αSMA was suppressed, calcific nodules did not form . Confoundingly, preventing phosphorylation of Erk1/2 with a MEK1/2 inhibitor leads to increased αSMA expression yet prevents calcific nodule formation , suggesting the requirement of another essential component of nodule formation that has yet to be revealed.
- Bioengineering Division
Cadherin-11 Regulates Calcific Nodule Formation by Aortic Valve Interstitial Cells
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Chen, J, Hutcheson, JD, Sewell-Loftin, MK, Ryzhova, LM, Fisher, CI, & Merryman, WD. "Cadherin-11 Regulates Calcific Nodule Formation by Aortic Valve Interstitial Cells." Proceedings of the ASME 2013 Summer Bioengineering Conference. Volume 1B: Extremity; Fluid Mechanics; Gait; Growth, Remodeling, and Repair; Heart Valves; Injury Biomechanics; Mechanotransduction and Sub-Cellular Biophysics; MultiScale Biotransport; Muscle, Tendon and Ligament; Musculoskeletal Devices; Multiscale Mechanics; Thermal Medicine; Ocular Biomechanics; Pediatric Hemodynamics; Pericellular Phenomena; Tissue Mechanics; Biotransport Design and Devices; Spine; Stent Device Hemodynamics; Vascular Solid Mechanics; Student Paper and Design Competitions. Sunriver, Oregon, USA. June 26–29, 2013. V01BT50A001. ASME. https://doi.org/10.1115/SBC2013-14201
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