| First Author | Mastrogiannaki M | Year | 2016 |
| Journal | J Invest Dermatol | Volume | 136 |
| Issue | 6 | Pages | 1130-42 |
| PubMed ID | 26902921 | Mgi Jnum | J:233454 |
| Mgi Id | MGI:5784794 | Doi | 10.1016/j.jid.2016.01.036 |
| Citation | Mastrogiannaki M, et al. (2016) beta-Catenin Stabilization in Skin Fibroblasts Causes Fibrotic Lesions by Preventing Adipocyte Differentiation of the Reticular Dermis. J Invest Dermatol 136(6):1130-42 |
| abstractText | The Wnt/beta-catenin pathway plays a central role in epidermal homeostasis and regeneration, but how it affects fibroblast fate decisions is unknown. We investigated the effect of targeted beta-catenin stabilization in dermal fibroblasts. Comparative gene expression profiling of stem cell antigen 1(-) (Sca1(-)) and Sca1(+) neonatal fibroblasts from upper and lower dermis, respectively, confirmed that Sca1(+) cells had a preadipocyte signature and showed differential expression of Wnt/beta-catenin-associated genes. By targeting all fibroblasts or selectively targeting Dlk1(+) lower dermal fibroblasts, we found that beta-catenin stabilization between developmental stages E16.5 and P2 resulted in a reduction in the dermal adipocyte layer with a corresponding increase in dermal fibrosis and an altered hair cycle. The fibrotic phenotype correlated with a reduction in the potential of Sca1(+) fibroblasts to undergo adipogenic differentiation ex vivo. Our findings indicate that Wnt/beta-catenin signaling controls adipogenic cell fate within the lower dermis, which potentially contributes to the pathogenesis of fibrotic skin diseases. |
