Publications by authors named "Chloe E Mirack"
The actin cytoskeleton is a potent regulator of tenocyte homeostasis. However, the mechanisms by which actin regulates tendon homeostasis are not entirely known. This study examined the regulation of tenocyte molecule expression by actin polymerization via the globular (G-) actin-binding transcription factor, myocardin-related transcription factor-a (MRTF).
View Article and Find Full Text PDFThe actin cytoskeleton is a potent regulator of tenocyte homeostasis. However, the mechanisms by which actin regulates tendon homeostasis are not entirely known. This study examined the regulation of tenocyte molecule expression by actin polymerization via the globular (G-) actin-binding transcription factor, myocardin-related transcription factor-a (MRTF).
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- 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