Hypermethylation of Frizzled1 is associated with Wnt/β-catenin signaling inactivation in mesenchymal stem cells of patients with steroid-associated osteonecrosis

Abstract

Bone disease: Signals from a modified gene Studies of genetic and molecular signaling processes in the bone disease osteonecrosis, when it is associated with steroid use, reveal insights into disease development and suggest new approaches for treatment. Steroid drugs increase the risk of osteonecrosis, in which bone tissue dies due to insufficient blood supply, but the mechanism of this effect is unclear. Researchers in China, led by Zhibo Sun at Wuhan University, investigated a link between the aberrant addition of methyl groups (CH3) to the DNA of a specific gene and the onset of the disease. They identified an important molecular signaling pathway in cultured bone marrow cells from patients that is inhibited by the gene methylation. Treating these cells with a drug that inhibits methylation led to reactivation of the gene and the associated signalling pathway that promotes healthy bone formation.