Dynamic reciprocity between fibroblasts and extracellular matrix in cardiomyopathy.
Department
Biological Sciences
Advisor
Jackie Towner
Document Type
Poster
Version
Metadata Only
Keywords:
Cardiomyopathy, Extracellular matrix
Abstract
Duchenne muscular dystrophy (DMD) is a degenerative muscular disease, resulting in chronic fibrosis that diminishes the effectiveness of contraction and repair in the heart and leads to heart failure and death. Fibrosis is an increased deposition of extracellular matrix (ECM) proteins that surround the cells in the heart. The ECM or matrix provides a microenvironment with dynamic reciprocity between the matrix and the cells interacting with it to influence cell behavior and proliferation. To study this interaction, we isolated the matrix from healthy three month old wild type mouse hearts and diseased hearts with DMD (mdx mouse model) and used the matrices as a scaffold for growing cells in vitro. One aspect of the dynamic reciprocity that occurs between the matrix and cells is the ability of cells to remodel the matrix by degrading or depositing matrix proteins. To measure this, we quantified the amount of laminin protein, a key matrix protein, by calculating the laminin remodeling index (LRI) using laminin immunofluorescence. We found a significant difference in the LRI of mdx matrices compared to wild type matrices, suggesting that a greater amount of cardiac remodeling occurs on mdx matrices than on wild type matrices.
Recommended Citation
Puumala, Eric; Knapp, Callie; Crosby, Rachelle; Hansen, Kirk; and Towner, Jackie, "Dynamic reciprocity between fibroblasts and extracellular matrix in cardiomyopathy." (2024). Science Symposium. 31.
https://spark.bethel.edu/science_symposium/spring2024/schedule2024/31
Terms of Use and License Information
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Dynamic reciprocity between fibroblasts and extracellular matrix in cardiomyopathy.
Duchenne muscular dystrophy (DMD) is a degenerative muscular disease, resulting in chronic fibrosis that diminishes the effectiveness of contraction and repair in the heart and leads to heart failure and death. Fibrosis is an increased deposition of extracellular matrix (ECM) proteins that surround the cells in the heart. The ECM or matrix provides a microenvironment with dynamic reciprocity between the matrix and the cells interacting with it to influence cell behavior and proliferation. To study this interaction, we isolated the matrix from healthy three month old wild type mouse hearts and diseased hearts with DMD (mdx mouse model) and used the matrices as a scaffold for growing cells in vitro. One aspect of the dynamic reciprocity that occurs between the matrix and cells is the ability of cells to remodel the matrix by degrading or depositing matrix proteins. To measure this, we quantified the amount of laminin protein, a key matrix protein, by calculating the laminin remodeling index (LRI) using laminin immunofluorescence. We found a significant difference in the LRI of mdx matrices compared to wild type matrices, suggesting that a greater amount of cardiac remodeling occurs on mdx matrices than on wild type matrices.