Biomechanical Remodeling of Aortic Valve Interstitial Cells During Calcified Lesion Formation In Vitro.
Justine Yushiuan ShihTerence GeeGaetano ScuderiJonathan T ButcherPublished in: Annals of biomedical engineering (2024)
Healthy aortic heart valves are essential to the regulation of unidirectional blood flow. Calcific aortic valve disease (CAVD) is an actively progressive disease that involves the disorganization of valve cells and accumulation of calcium deposits on the aortic valve leaflets. CAVD involves disruption of cell environment homeostasis that prior cell culture models have found difficult to portray and model. As it is still poorly understood how tissue stiffening associates with lesion formation, here, we implement a novel 3D culture platform to characterize the relationship between mechanical stress and tissue remodeling and analyze how the application of pro-osteogenic stimulation dysregulates the native ability of valve cells to organize its matrix. Through a temporal study of macroscopic remodeling, we determine that aortic valve interstitial neo-tissues undergo varying stiffness and mechanical stress, demonstrate greater myofibroblastic gene expression, and show greater remodeling activity in the outer surface of the neo-tissue in a banding pattern when cultured in osteogenic growth medium. In human aortic valve interstitial cells cultured in osteogenic growth medium, we observed an increase in stress but significant decreases in myofibroblastic gene expression with the addition of growth factors. In summary, we are able to see the interplay of biochemical and biomechanical stimuli in valvular remodeling by using our platform to model dynamic stiffening of valve interstitial neo-tissues under different biochemical conditions.
Keyphrases
- aortic valve
- transcatheter aortic valve replacement
- aortic stenosis
- transcatheter aortic valve implantation
- aortic valve replacement
- gene expression
- induced apoptosis
- cell cycle arrest
- mesenchymal stem cells
- endothelial cells
- bone marrow
- blood flow
- heart failure
- dna methylation
- cell death
- endoplasmic reticulum stress
- oxidative stress
- stem cells
- high throughput