MATRIX EXPRESSION IN PASSAGED CHONDROCYTES IS REGULATED BY TROPOMYOSIN 3.1
| Author(s) | Rzepski, Alissa | |
| Date Accessioned | 2024-06-12T19:48:00Z | |
| Date Available | 2024-06-12T19:48:00Z | |
| Publication Date | 2023-05 | |
| Abstract | Cartilage is an avascular tissue that allows frictionless mobility of joints. Cartilage cells (chondrocytes) reside in a matrix of collagens (type II collagen [Col2]) and proteoglycans (aggrecan [Acan]) to bear mechanical load [2, 10, 14]. Unfortunately, cartilage is incapable of self-repair and damage leads to cartilage degradation in osteoarthritis (OA). Autologous chondrocyte implantation (ACI) is used to treat small, focal cartilage defects. Chondrocytes are isolated from healthy regions of cartilage in damaged joints, expanded on stiff polystyrene to increase number, then reimplanted into damaged regions to stimulate repair. Unfortunately, ACI ultimately fails [9, 18, 20, 23]. During expansion, chondrocytes become larger, elongated, and express fibroblastic matrix (type I collagen [Col1]) and contractile (transgelin [Tagln]) molecules, which are biomechanically inferior [2, 14, 22, 23, 39, 41, 43]. Additionally, cellular filamentous (F-)actin organization changes from cortical F actin to F-actin stress fibers. Our previous research indicates formation of F-actin stress fibers plays a key role in chondrocyte dedifferentiation [1]. In the present study, we examined ways to repress F-actin stress fiber formation by examining master regulators of actin networks, the Tropomyosins (Tpm), which bind and stabilize specific F-actinnetworks [32, 41]. Therefore, we hypothesize that targeting specific stress fiber actin stabilizing Tpms will repress F-actin stress fiber networks and promote chondrogenic redifferentiation after expansion. | |
| Advisor | enter | |
| Program | enter | |
| URL | https://udspace.udel.edu/handle/19716/34498 | |
| Language | en_US | |
| Publisher | University of Delaware | |
| Title | MATRIX EXPRESSION IN PASSAGED CHONDROCYTES IS REGULATED BY TROPOMYOSIN 3.1 | |
| Type | Thesis |
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