Logo image
Calcium Signaling Regulates Valvular Interstitial Cell Alignment and Myofibroblast Activation in Fast-relaxing Boronate Hydrogels
Journal article   Peer reviewed

Calcium Signaling Regulates Valvular Interstitial Cell Alignment and Myofibroblast Activation in Fast-relaxing Boronate Hydrogels

Hao Ma, Laura J. Macdougall, Andrea Gonzalez Rodriguez, Megan E. Schroeder, Dilara Batan, Robert M. Weiss and Kristi S. Anseth
Macromolecular bioscience, Vol.20(12), pp.e2000268-e2000268
09/13/2020
DOI: 10.1002/mabi.202000268
PMCID: PMC7773027
PMID: 32924320

View Online

Abstract

The role viscoelasticity plays in fibrotic disease progression is an emerging area of interest. Here, a fast-relaxing hydrogel system is exploited to investigate potential crosstalk between calcium signaling and mechanotransduction. Poly(ethylene glycol) (PEG) hydrogels containing boronate and triazole crosslinkers are synthesized, with varying ratios of boronate to triazole crosslinks to systematically vary the extent of stress relaxation in the final hydrogel formulation. Valvular interstitial cells (VICs) are encapsulated in these fast-relaxing scaffolds, and the role that viscoelasticity plays on VIC alignment and myofibroblast activation is investigated. VICs cultured in hydrogels with the highest levels of stress relaxation (90%) exhibit a spread morphology by day 1 and are highly aligned (80 ± 2 %) by day 5. Key myofibroblast markers, including α-smooth muscle actin (αSMA) and collagen 1a1 (COLL1A1), are also significantly elevated. VIC myofibroblast activation decreases by 42 ± 18% through inhibition of mechanotransduction, independently of VIC morphology and alignment. Calcium signaling through a transient receptor potential vanilloid 4 (TRPV4) is found to regulate VIC spreading, alignment, and myofibroblast activation in a time dependent manner. Inhibition of calcium signaling at early time points results in disturbed cell alignment, decreased mechanotransduction, and diminished myofibroblast activation, while inhibition at later time points only causes partially reduced myofibroblast activation. These results suggest a potential crosstalk mechanism between calcium signaling and mechanotransduction, where calcium signaling acts upstream of mechanosensing and can interestingly also regulate VIC myofibroblast activation independently of mechanotransduction. Valvular interstitial cell (VIC) alignment and myofibroblast activation was investigated in a 3D fast-relaxing hydrogel scaffold with tunable viscoelasticity. VIC spreading and alignment correlated with higher extents of matrix viscoelasticity and stress relaxation via activating calcium channels. A potential crosstalk between viscoelasticity, calcium signaling, and mechanotransduction was proposed, which provides new insights into potential targets for valvular tissue fibrosis treatment.
3D hydrogels boronate chemistries mechanotransduction myofibroblasts valvular interstitial cells

Details

Metrics

Logo image