Does rapamycin-Induced Hypoxia Inducible Factor 2A be Essential for Chondrogenic Differentiation of Amniotic Fluid Stem Cells?
Repair of cartilage defects is still an unresolved issue in regenerative medicine. Results of this study showed that inhibition of the mammalian target of rapamycin complex 1 (mTORC1) pathway, by rapamycin or by small interfering RNA-mediated targeting of raptor (gene name, RPTOR), enhanced amniotic fluid stem cell differentiation toward a chondrocytic phenotype and increased their engrafting efficiency into cartilaginous structures. Moreover, freshly isolated and in vitro passaged human chondrocytes also showed redifferentiation upon mTORC1 inhibition during culturing. Therefore, this study revealed that rapamycin could enable a more efficient clinical use of cell-based therapy approaches to treat articular cartilage defects.
We conclude that CD4+ T cells from mesenteric lymph nodes of mice with allergen-induced immediate-type hypersensitivity reactions in the gut are able to transfer the phenotype of experimental asthma.