Publications by authors named "Mandy M Schofield"
Article Synopsis
- Actin plays a crucial role in maintaining the chondrocyte phenotype, but monolayer expansion for cell-based therapies causes chondrocytes to dedifferentiate, altering their actin structure and reducing cartilage matrix expression.* -
- This study focuses on the roles of tropomyosin (TPM3.1) and RhoGTPase (CDC42) in regulating F-actin networks and chondrocyte phenotype during dedifferentiation and passaging.* -
- Results show that inhibiting TPM3.1 or CDC42 leads to reorganization of F-actin back to a more differentiated state, indicated by reduced fibroblastic matrix expression and increased expression of chondrogenic factors like SO
Actin is a central mediator of the chondrocyte phenotype. Monolayer expansion of articular chondrocytes on tissue culture polystyrene, for cell-based repair therapies, leads to chondrocyte dedifferentiation. During dedifferentiation, chondrocytes spread and filamentous (F-)actin reorganizes from a cortical to a stress fiber arrangement causing a reduction in cartilage matrix expression and an increase in fibroblastic matrix and contractile molecule expression.
View Article and Find Full Text PDFActin is a central mediator between mechanical force and cellular phenotype. In tendons, it is speculated that mechanical stress deprivation regulates gene expression by reducing filamentous (F)-actin. However, the mechanisms regulating tenocyte F-actin remain unclear.
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