Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Active tissue stiffness modulation controls valve interstitial cell phenotype and osteogenic potential in 3D culture.

Acta biomaterialia - 1 May 2016

Duan Bin, Yin Ziying, Hockaday Kang Laura, Magin Richard L, Butcher Jonathan T

Abstract excerpt

UNLABELLED: Calcific aortic valve disease (CAVD) progression is a highly dynamic process whereby normally fibroblastic valve interstitial cells (VIC) undergo osteogenic differentiation, maladaptive extracellular matrix (ECM) composition, structural remodeling, and tissue matrix stiffening. However, how VIC with different phenotypes dynamically affect matrix properties and how the altered matrix further affects...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aortic Valve
Share to Biomechanical Phenomena

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cross-Linking Reagents

Share to Hydrogels

Share to Myofibroblasts

Share to Osteogenesis

Share to rho-Associated Kinases

Share to rhoA GTP-Binding Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 26947381
DOI: 10.1016/j.actbio.2016.03.007
PMCID: PMC4883663

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Active tissue stiffness modulation controls valve interstitial cell phenotype and osteogenic potential in 3D culture.PMID 26947381Read ↗

Simulation of early calcific aortic valve disease in a 3D platform: A role for myofibroblast differentiation.Semantic proximity Read ↗

Calcification by valve interstitial cells is regulated by the stiffness of the extracellular matrix.Semantic proximity Read ↗

The progression of calcific aortic valve disease through injury, cell dysfunction, and disruptive biologic and physical force feedback loops.Semantic proximity Read ↗

Hydrogels preserve native phenotypes of valvular fibroblasts through an elasticity-regulated PI3K/AKT pathway.Semantic proximity Read ↗

TRPV4-mediated Mechanotransduction Regulates the Differentiation of Valvular Interstitial Cells to Myofibroblasts: Implications for Aortic StenosisSemantic proximity Read ↗

The Roles of Matrix Stiffness and ß-Catenin Signaling in Endothelial-to-Mesenchymal Transition of Aortic Valve Endothelial Cells.Semantic proximity Read ↗

The role of valvular endothelial cell paracrine signaling and matrix elasticity on valvular interstitial cell activation.Semantic proximity Read ↗

TRPV4 calcium-permeable channel contributes to valve stiffening in aortic stenosisSemantic proximity Read ↗

Manipulation of valve composition to elucidate the role of collagen in aortic valve calcification.Semantic proximity Read ↗

Regulation of valvular interstitial cell phenotype and function by hyaluronic acid in 2-D and 3-D culture environments.Semantic proximity Read ↗

Spatiotemporal Multi-Omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving DiseaseSemantic proximity Read ↗

3D Contractile and Remodeling Behaviors of Functionally Normal and Prolapsed Human Mitral Valve Interstitial CellsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.