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Isolation of Human Primary Valve Cells for In vitro Disease Modeling
Published on: April 16, 2021
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Surface chemistry regulates valvular interstitial cell differentiation in vitro.
Matthew N Rush1, Kent E Coombs2, Elizabeth L Hedberg-Dirk3
1Center for Biomedical Engineering, University of New Mexico, Albuquerque, NM, USA; Nanoscience and Microsystems Engineering, University of New Mexico, Albuquerque, NM, USA.
Acta Biomaterialia
|October 3, 2015
Summary
Substrate surface chemistry influences valvular interstitial cell (VIC) differentiation and calcification, offering new in vitro models for studying valvular heart disease and developing therapeutics.
Area of Science:
- Biomaterials Science
- Cell Biology
- Cardiovascular Research
Background:
- Valvular calcification, driven by valvular interstitial cell (VIC) differentiation, is a significant risk factor for mortality and cardiovascular disorders.
- The precise factors initiating osteoblastic-like VICs (obVICs) and subsequent calcification remain incompletely understood.
- Understanding these mechanisms is crucial for developing effective treatments for calcified valve stenosis.
Purpose of the Study:
- To investigate the impact of substrate surface chemistry on VIC differentiation and calcified tissue formation in vitro.
- To determine if surface chemistry alone can induce VICs to adopt an osteoblastic phenotype and form calcified tissue.
- To identify novel in vitro models for studying valvular calcification and testing potential therapeutics.
Main Methods:
- Utilized self-assembled monolayers (SAMs) with varying surface chemistries (CH3, OH, COOH, NH2) on gold substrates.
- Cultured VICs on these functionalized SAMs for seven days to observe differentiation and calcification.
- Analyzed cell proliferation, morphology, osteoblastic marker expression (osteocalcin, α-smooth muscle actin), and nodule formation.
Main Results:
- Surface chemistry significantly modulated VIC proliferation, morphology, and osteoblastic potential.
- NH3(+)- and CH3-terminated SAMs promoted calcified tissue formation, while COO(-)-terminated SAMs did not.
- VICs on NH3(+)-SAMs showed robust osteoblastic markers and nodule formation; VICs on CH3-SAMs exhibited dystrophic calcification characteristics.
- Surface-induced calcification differed from media-induced calcification, highlighting the role of the material interface.
Conclusions:
- Substrate surface chemistry is a critical factor in altering VIC behavior and driving calcified tissue formation independently of soluble factors.
- Identified two novel in vitro mechanisms for inducing calcified VICs using specific surface chemistries.
- These findings provide new avenues for studying valvular heart disease pathogenesis and developing in vitro drug screening platforms.
