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Age-related wild type transthyretin amyloidosis is characterized by systemic deposition of amyloidogenic fibrils of misfolded transthyretin in the connective cells of many organs. The theory evaluated is that TTR impacts cardiac fibroblasts in means that might add to fibrosis. When main cardiac fibroblasts were cultured on TTR-deposited substrates, the F-actin cytoskeleton disordered, focal bond formation lowered, and nuclear form was squashed. Together, results suggest that TTR transferred in tissue extracellular matrix might influence both the structure, gene and function expression of cardiac fibroblasts. Total layout: Three samples of cardiac fibroblasts expanded on both neglected and TTR fibril-containing substratums.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/734300
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