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Isolation of Human Primary Valve Cells for In vitro Disease Modeling
Published on: April 16, 2021
Correlation between heart valve interstitial cell stiffness and transvalvular pressure: implications for collagen
W David Merryman1, Inchan Youn, Howard D Lukoff
1Dept. of Bioengineering, Univ. of Pittsburgh, Pittsburgh, PA 15219, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|August 30, 2005
Summary
Heart valve interstitial cells (VICs) stiffen and increase collagen production under higher pressure, maintaining tissue balance. This stress-response mechanism is key to understanding valve health and disease.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanics
- Biomaterials Science
Background:
- Heart valve interstitial cells (VICs) are crucial for valvular tissue homeostasis, regulating extracellular matrix biosynthesis.
- VICs exhibit phenotypic plasticity, differentiating into myofibroblasts during development and disease.
- Significant differences exist in transvalvular pressures (TVPs) between the left and right sides of the heart.
Purpose of the Study:
- To investigate the hypothesis that higher left-side TVPs increase VIC stiffness and affect collagen biosynthesis.
- To explore the relationship between mechanical stress, cellular stiffness, and matrix production in VICs.
- To understand the role of VICs in maintaining valvular tissue homeostasis under varying pressure conditions.
Main Methods:
- Isolated ovine VICs from all four heart valves were subjected to micropipette aspiration to measure cellular stiffness.
- Cytoskeletal composition (using smooth muscle alpha-actin, SMA) and collagen biosynthesis (using heat shock protein 47, HSP47) were quantified.
- In vitro and in situ assays were performed to compare VIC properties between left and right heart valves.
Main Results:
- VICs from the aortic and mitral valves (left side) were significantly stiffer than those from the pulmonary and tricuspid valves (right side).
- Left-side VICs exhibited higher levels of SMA and HSP47 compared to right-side VICs.
- VIC stiffness correlated strongly with TVP, and SMA levels correlated with HSP47, indicating a stress-dependent response.
Conclusions:
- VICs adapt to local tissue stress by altering cellular stiffness, influenced by SMA content.
- Increased cellular stiffness and collagen biosynthesis in VICs are linked to higher transvalvular pressures.
- This stress-dependent relationship in VICs is vital for maintaining valvular tissue homeostasis and understanding valve pathologies.
