Hmga2 promotes the development of myelofibrosis in Jak2^V617F knockin mice by enhancing TGF-β1 and Cxcl12 pathways.

ABSTRACT: Myelofibrosis (MF) is a devastating blood disorder. The JAK2V617F mutation has been detected in ∼50% cases of MF. Elevated expression of high-mobility group AT hook 2 (HMGA2) has also been frequently observed in patients with MF. Interestingly, upregulation of HMGA2 expression has been found in association with the JAK2V617F mutation in significant cases of MF. However, the contribution of HMGA2 in the pathogenesis of MF remains elusive. To determine the effects of concurrent expression of HMGA2 and JAK2V617F mutation in hematopoiesis, we transduced bone marrow cells from Jak2^V617F knockin mice with lentivirus expressing Hmga2 and performed bone marrow transplantation. Expression of Hmga2 enhanced megakaryopoiesis, increased extramedullary hematopoiesis, and

SUBMITTER: Dutta A 

PROVIDER: S-EPMC5561898 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature