Title of article :
Substrate elasticity controls cell proliferation, surface marker expression and motile phenotype in amniotic fluid-derived stem cells
Author/Authors :
Aleksander Skardal، نويسنده , , Aleksander and Mack، نويسنده , , David and Atala، نويسنده , , Anthony and Soker، نويسنده , , Shay، نويسنده ,
Issue Information :
ماهنامه با شماره پیاپی سال 2013
Pages :
10
From page :
307
To page :
316
Abstract :
The physical cues presented to stem cells by the substrate on or in which they exist have been shown to play a crucial role in regulation of their behavior. Until recently, most research has focused on the effects of substrate elasticity on differentiation capability rather than maintenance of long-term proliferation and plasticity. The main goal of the present study is to study the interaction of amniotic fluid-derived stem (AFS) cells with growth substrata of different elasticity, which may extend their application potentials. Here, we investigate the effects of elastic modulus (E′), on AFS cell proliferation, morphology, cell surface marker expression, and autocrine stimulation of cell migration. AFS cells cultured on substrates of different E′ exhibited significant changes in proliferation and morphology. Immunohistochemistry revealed increased expression of cell surface markers associated with mesenchymal stem cells (MSCs) (CD44, CD90, CD105, and N-cadherin) in cells cultured on softer substrates. Additionally, AFS cells cultured on softer substrates induced autocrine stimulation of migration. Therefore, tailoring the elastic modulus of biomaterials to specific stiffness values is an effective method to control stem cell properties, which may modulate the effectiveness of their therapeutic applications.
Keywords :
cell therapy , Cell mobility , Elastic modulus , biomaterial , amniotic fluid-derived stem cells
Journal title :
Journal of the Mechanical Behavior of Biomedical Materials
Serial Year :
2013
Journal title :
Journal of the Mechanical Behavior of Biomedical Materials
Record number :
1405787
Link To Document :
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