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  • Interstitial Cell Remodeling Promotes Aberrant Adipogenesis in Dystrophic Muscles.

Interstitial Cell Remodeling Promotes Aberrant Adipogenesis in Dystrophic Muscles.

Cell reports (2020-05-07)
Jordi Camps, Natacha Breuls, Alejandro Sifrim, Nefele Giarratana, Marlies Corvelyn, Laura Danti, Hanne Grosemans, Sebastiaan Vanuytven, Irina Thiry, Marzia Belicchi, Mirella Meregalli, Khrystyna Platko, Melissa E MacDonald, Richard C Austin, Rik Gijsbers, Giulio Cossu, Yvan Torrente, Thierry Voet, Maurilio Sampaolesi
ABSTRACT

Fibrosis and fat replacement in skeletal muscle are major complications that lead to a loss of mobility in chronic muscle disorders, such as muscular dystrophy. However, the in vivo properties of adipogenic stem and precursor cells remain unclear, mainly due to the high cell heterogeneity in skeletal muscles. Here, we use single-cell RNA sequencing to decomplexify interstitial cell populations in healthy and dystrophic skeletal muscles. We identify an interstitial CD142-positive cell population in mice and humans that is responsible for the inhibition of adipogenesis through GDF10 secretion. Furthermore, we show that the interstitial cell composition is completely altered in muscular dystrophy, with a near absence of CD142-positive cells. The identification of these adipo-regulatory cells in the skeletal muscle aids our understanding of the aberrant fat deposition in muscular dystrophy, paving the way for treatments that could counteract degeneration in patients with muscular dystrophy.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
bisBenzimide H 33342 trihydrochloride, for fluorescence, ≥97.0% (HPLC)
Sigma-Aldrich
Anti-Laminin antibody produced in rabbit, 0.5 mg/mL, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
MISSION® esiRNA, targeting human GDF10
Sigma-Aldrich
Anti-Rabbit IgG (H+L), CF488A F(ab′)2 fragment of antibody produced in goat, ~2 mg/mL, affinity isolated antibody, buffered aqueous solution