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| Status |
Public on Dec 29, 2022 |
| Title |
Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
We developed an on-slide decellularization approach to generate acellular extracellular matrix (ECM) scaffolds that can be repopulated with various cell types to interrogate cell-ECM interactions. Using this platform, we investigated whether fibrotic ECM scarring affected human skeletal muscle progenitor cell (SMPC) functions that are essential for myoregeneration. SMPCs exhibited robust adhesion, motility, and differentiation on healthy muscle-derived myoscaffolds. All SPMC interactions with fibrotic myoscaffolds from dystrophic muscle were severely blunted including reduced motility rate and migration. Furthermore, SMPCs were unable to remodel laminin dense fibrotic scars within diseased myoscaffolds. Proteomics and structural analysis revealed that excessive collagen deposition alone is not pathological, and can be compensatory, as revealed by overexpression of sarcospan and its associated ECM receptors in dystrophic muscle. Our in vivo data also supported that ECM remodeling is important for SMPC engraftment and that fibrotic scars may represent one barrier to efficient cell therapy.
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| |
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| Overall design |
Sequencing pf total RNA prepared from SMPCs cultured (5 days) on WT and mdx myoscaffolds.
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| Contributor(s) |
Stearns-Reider KM, Crosbie RH |
| Citation(s) |
36922514 |
| |
| Submission date |
Dec 29, 2022 |
| Last update date |
Jul 14, 2023 |
| Contact name |
Yerbol Z. Kurmangaliyev |
| Organization name |
University of California, Los Angeles
|
| Street address |
675 Charles E. Young Drive South
|
| City |
Los Angeles |
| State/province |
CA |
| ZIP/Postal code |
90095 |
| Country |
USA |
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| Platforms (1) |
| GPL21290 |
Illumina HiSeq 3000 (Homo sapiens) |
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| Samples (5)
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| Relations |
| BioProject |
PRJNA916716 |
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