8 research outputs found
ISG15 Modulates Development of the Erythroid Lineage
Activation of erythropoietin receptor allows erythroblasts to generate erythrocytes. In a search for genes that are up-regulated during this differentiation process, we have identified ISG15 as being induced during late erythroid differentiation. ISG15 belongs to the ubiquitin-like protein family and is covalently linked to target proteins by the enzymes of the ISGylation machinery. Using both in vivo and in vitro differentiating erythroblasts, we show that expression of ISG15 as well as the ISGylation process related enzymes Ube1L, UbcM8 and Herc6 are induced during erythroid differentiation. Loss of ISG15 in mice results in decreased number of BFU-E/CFU-E in bone marrow, concomitant with an increased number of these cells in the spleen of these animals. ISG15-/- bone marrow and spleen-derived erythroblasts show a less differentiated phenotype both in vivo and in vitro, and over-expression of ISG15 in erythroblasts is found to facilitate erythroid differentiation. Furthermore, we have shown that important players of erythroid development, such as STAT5, Globin, PLC γ and ERK2 are ISGylated in erythroid cells. This establishes a new role for ISG15, besides its well-characterized anti-viral functions, during erythroid differentiation
The temporal organisation of the feeding behaviour of four species of wallaby: examining chronobiological and homeostatic influences
Continuous Fli-1 expression plays an essential role in the proliferation and survival of F-MuLV-induced erythroleukemia and human erythroleukemia
Intra-coronary morphine versus placebo in the treatment of acute ST-segment elevation myocardial infarction: the MIAMI randomized controlled trial
Stem Cell-Based and Tissue Engineering Approaches for Skeletal Muscle Repair
Skeletal muscle tissue exhibits significant regeneration capacity upon injury or disease. This intrinsic regeneration potential is orchestrated by stem cells termed satellite cells, which undergo activation and differentiation in response to muscle insult, giving rise to fusion-competent myogenic progenitors responsible for tissue rejuvenation. Skeletal muscle diseases such as Duchenne muscular dystro-phy are characterized by progressive loss of muscle mass which precipitates reduced motility, paralysis, and in some occurrences untimely death. A manifold of muscle pathologies involve a failure to efficiently regenerate the muscle tissue, rendering stem cell-based approaches an attractive therapeutic strategy. Here we will present past and contemporary methods to treat skeletal muscle degeneration by stem cell therapy, covering prominent challenges facing this technology and potential means to overcome current hurdles. A primary focus of this chapter is directed toward illustrating innovative ways to utilize stem cells alone or in conjunction with biomaterials and tissue engineering techniques to remedy Duchenne muscular dystrophy or volumetric muscle loss