Substrate elasticity regulates adipose-derived stromal cell differentiation towards osteogenesis and adipogenesis through β-catenin transduction.
Xie J., Zhang D., Zhou C., Yuan Q., Ye L., Zhou X.
Animal Study, published in Acta Biomater (2018) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Acta Biomater (2018)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30134207
- DOI
- 10.1016/j.actbio.2018.08.018
- Citations
- 73
Abstract (original English)
It is generally recognised that mesenchymal stem cells (MSCs) can differentiate into multiple lineages through guidance from the biophysical properties of the substrates. However, the precise biophysical mechanism that enables MSCs to respond to substrate properties remains unclear. In the current study, polydimethylsiloxane (PDMS) substrates with different stiffnesses were fabricated and the way in which the elastic modulus of the substrate regulated differentiation towards osteogenesis and adipogenesis in adipose-derived stromal cells (ASCs) was explored. Initially, a cell morphology change by SEM was observed between the stiff and soft substrates. The cytoskeleton stains including microfilament by F-actin and microtubule by α- and β-tubulin further showed a larger cell spreading area on the stiff substrate. Then the expression of vinculin, in charge for the linkage of adhesion molecules to the actin cytoskeleton, was enhanced on the stiff substrate. This change in focal adhesion plaque further triggered intracellular β-catenin signaling and promoted its nuclear translocation especially on the stiff substrate. The influence of β-catenin signaling on direct differentiation to osteogenic lineages was through direct binding between its downstream protein, Lef-1, and the osteogenic transcriptional factors, Runx2 and Osx, while on differentiation to adipogenic lineages was through
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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