Intact cholesterol metabolic balance, help maintain hematopoietic stem cells and multi-progenitor cells (HSPC) in the resting state. Cross the cell membrane transporter cholesterol adenosine triphosphate-binding cassette transporter factors ABCA1 and ABCG1 defects can lead to the mouse cell cholesterol efflux pathway barriers.

Such mice showed a dramatic increase in HSPC mobilization and extramedullary hematopoiesis. The extramedullary hematopoiesis dramatic increase is caused due to splenic macrophages and dendritic cells to produce IL-2-induced increase in serum G-CSF levels.

The extramedullary hematopoiesis increase to promote the differentiation of bone marrow hematopoietic lineages decided to granulocytes, and not inclined to the direction of the macrophage differentiation. This damages the support of the osteoblasts and mesenchymal progenitor the cells produce Cxcl12/SDF-1 factor reduction.

Increased high-density lipoprotein levels the Abca1-/-Abcg1-/- and ApoE-/ - mice and FLT3-ITD mutation-mediated myeloproliferative neoplasms in the mouse model, a strong mobilization of HSPC and extramedullary hematopoiesis the reversal. Of FLT3 (FMS-like tyrosine kinase, of FMS-like tyrosine kinase 3) belongs to the type III receptor tyrosine kinase (receptor tyrosine kinase III, RTK III) family members, In recent years, many studies have demonstrated large sample of FLT3 activation mutations play an important pathological role in the occurrence and progression of the disease in AML.

The data of this study is to determine the cholesterol efflux pathway HSPC mobilization has control. This is likely to translate into atherosclerosis and treatment strategies for hematologic malignancies.

Hide Comments | Add Comment