| First Author | Takada N | Year | 2022 |
| Journal | Development | Volume | 149 |
| Issue | 3 | PubMed ID | 35029658 |
| Mgi Jnum | J:321946 | Mgi Id | MGI:6886137 |
| Doi | 10.1242/dev.199443 | Citation | Takada N, et al. (2022) Galectin-3 promotes the adipogenic differentiation of PDGFRalpha+ cells and ectopic fat formation in regenerating muscle. Development 149(3):dev199443 |
| abstractText | Worldwide prevalence of obesity is associated with the increase of lifestyle-related diseases. The accumulation of intermuscular adipose tissue (IMAT) is considered a major problem whereby obesity leads to sarcopenia and metabolic disorders and thus is a promising target for treating these pathological conditions. However, whereas obesity-associated IMAT is suggested to originate from PDGFRalpha+ mesenchymal progenitors, the processes underlying this adipogenesis remain largely unexplored. Here, we comprehensively investigated intra- and extracellular changes associated with these processes using single-cell RNA sequencing and mass spectrometry. Our single-cell RNA sequencing analysis identified a small PDGFRalpha+ cell population in obese mice directed strongly toward adipogenesis. Proteomic analysis showed that the appearance of this cell population is accompanied by an increase in galectin-3 in interstitial environments, which was found to activate adipogenic PPARgamma signals in PDGFRalpha+ cells. Moreover, IMAT formation during muscle regeneration was significantly suppressed in galectin-3 knockout mice. Our findings, together with these multi-omics datasets, could unravel microenvironmental networks during muscle regeneration highlighting possible therapeutic targets against IMAT formation in obesity. |
