Journal
CELL REPORTS
Volume 27, Issue 7, Pages 2029-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.04.074
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Funding
- Glenn Foundation for Aging Research
- NIH [T32 AG000266, K99 AG053438, P01 AG036695, TR01 AG047820]
- NIH (R37 (MERIT Award)) [AG023806]
- Department of Veterans Affairs (BLRD Merit Review)
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The necessity of mesenchymal stromal cells, called fibroadipogenic progenitors (FAPs), in skeletal muscle regeneration and maintenance remains unestablished. We report the generation of a PDGFR alpha(creER) knockin mouse model that provides a specific means of labeling and targeting FAPs. Depletion of FAPs using Cre-dependent diphtheria toxin expression results in loss of expansion of muscle stem cells (MuSCs) and CD45+ hematopoietic cells after injury and impaired skeletal muscle regeneration. Further-more, FAP-depleted mice under homeostatic conditions exhibit muscle atrophy and loss of MuSCs, revealing that FAPs are required for the maintenance of both skeletal muscle and the MuSC pool. We also report that local tamoxifen metabolite delivery to target CreER activity in a single muscle, removing potentially confounding systemic effects of ablating PDGFR alpha+ cells distantly, also causes muscle atrophy. These data establish a critical role of FAPs in skeletal muscle regeneration and maintenance.
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