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Status |
Public on Apr 11, 2013 |
Title |
Type 2 innate signals regulate functionality of fibro/adipogenic progenitors to facilitate muscle regeneration |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
In vertebrates, activation of innate immunity is an early response to injury, implicating it in the regenerative process. However, the mechanisms by which innate signals might regulate stem cell functionality are unknown. Here we demonstrate that type 2 innate immunity is required for regeneration of skeletal muscle after injury. Muscle damage results in rapid recruitment of eosinophils, which secrete IL-4 to activate the regenerative actions of muscle resident fibro/adipocyte progenitors (FAPs). In FAPs, IL-4/IL-13 signaling serves as a key switch to control their fate and functions. Activation of IL-4/IL-13 signaling promotes proliferation of FAPs to support myogenesis, while inhibiting their differentiation into adipocytes. Surprisingly, type 2 cytokine signaling is also required in FAPs, but not myeloid cells, for rapid clearance of necrotic debris, a process that is necessary for timely and complete regeneration of tissues.
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Overall design |
Fibroadipocyte progenitors were isolated from wild-type and IL-4Ra knockout (IL-4Ra -/-) mice and were treated with vehicle or IL4 stimulation in culture prior to microarray analysis. 4 biological replicates of each condition were performed.
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Contributor(s) |
Deo RC, Heredia JE, Mukundan L, Chen FM, Mueller AA, Locksley RM, Rando TA, Chawla A |
Citation(s) |
23582327 |
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Submission date |
Mar 06, 2013 |
Last update date |
Jun 14, 2018 |
Contact name |
Rahul C Deo |
E-mail(s) |
[email protected]
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Organization name |
University of California San Francisco
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Department |
Cardiovascular Research Institute
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Lab |
Deo
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Street address |
555 Mission Bay Blvd. South
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City |
SAN FRANCISCO |
State/province |
CA |
ZIP/Postal code |
94158 |
Country |
USA |
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Platforms (1) |
GPL6885 |
Illumina MouseRef-8 v2.0 expression beadchip |
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Samples (16)
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Relations |
BioProject |
PRJNA192620 |