Modulation of host cell mechanics byTrypanosoma cruzi
Autor: | Adam Mott, Barbara A. Burleigh, Jeffrey J. Fredberg, Jaime A. Costales, Guillaume Lenormand |
---|---|
Rok vydání: | 2009 |
Předmět: |
Male
Myosin Light Chains Time Factors Physiology Trypanosoma cruzi Clinical Biochemistry Context (language use) Article Host-Parasite Interactions Depsipeptides Animals Humans Phosphorylation Cytoskeleton Protein kinase A Rho-associated protein kinase Actin rho-Associated Kinases biology Cell Biology Mechanics Fibroblasts biology.organism_classification Cyclic AMP-Dependent Protein Kinases Actins Biomechanical Phenomena Cell biology Signal transduction Intracellular |
Zdroj: | Journal of Cellular Physiology. 218:315-322 |
ISSN: | 1097-4652 0021-9541 |
DOI: | 10.1002/jcp.21606 |
Popis: | To investigate the effects of Trypanosoma cruzi on the mechanical properties of infected host cells, cytoskeletal stiffness and remodeling dynamics were measured in parasite-infected fibroblasts. We find that cell stiffness decreases in a time-dependent fashion in T. cruzi-infected human foreskin fibroblasts without a significant change in the dynamics of cytoskeletal remodeling. In contrast, cells exposed to T. cruzi secreted/released components become significantly stiffer within two hours of exposure and exhibit increased remodeling dynamics. These findings represent the first direct mechanical data to suggest a physical picture in which an intact, stiff, and rapidly remodeling cytoskeleton facilitates early stages of T. cruzi invasion and parasite retention, followed by subsequent softening and disassembly of the cytoskeleton to accommodate intracellular replication of parasites. We further suggest that these changes occur through protein kinase A and inhibition of the Rho/Rho kinase signaling pathway. In the context of tissue infection, changes in host cell mechanics could adversely affect the function of the infected organs, and may play an important role on the pathophysiology of Chagas' disease. |
Databáze: | OpenAIRE |
Externí odkaz: |