논문 상세보기

Effects of FGF2 in hematopoietic stem cell proliferation in bone marrow

  • 언어ENG
  • URLhttps://db.koreascholar.com/Article/Detail/354651
서비스가 종료되어 열람이 제한될 수 있습니다.
한국발생생물학회 (The Korea Society Of Developmental Biology)
초록

Hematopoietic stem cells (HSCs) can self-renew and can differentiate to a variety of specialized blood cells). The proliferation and homing of HSCs are strictly regulated both in the system level and local level. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic growth factor, potent species-specific stimulator of granulocyte-macrophage, eosinophil, megakaryocyte and erythroid progenitors. In clinical purpose GM-CSF has been used as hematopoietic growth factor. It can promote the mobilization of HSC from bone marrow to peripheral blood. The number of HSCs mobilized into blood can be modulated by the kinds of cytolines. However, the information for the cytokine which promote mobilization is limited. Basic fibroblast growth factor (bFGF or FGF-2) induces the change of niche and affects the maintenance and differentiation of HSCs. FGF-2 positively regulates hematopoiesis, by acting on stroma cells, on early and committed hematopoietic progenitors, and possibly on some mature blood cells. In this study, we investigated the effect of FGF-2 on HSCs mobilization and proliferation compare to GM-CSF. GM-CSF and FGF-2 were injected for 2 or 5 days into peritoneum of CD-1 mice (6~8 wks old) and sampling the bone marrow and peripheral blood. The bone marrow cells and peripheral blood were analyzed using FACS. In GM-CSF group, the number of HSCs was significantly increased by 2 days of injection but was significantly decreased in 5 days of injection. On the other hand the number of HSCs was significantly increased by the administration of FGF2 both in 2 days and 5 days. GM-CSF and FGF-2 are all increased the number of HSC both in bone marrow and peripheral blood. From these results, it is revealed that chronic administration of GM-CSF does not cause of the increase the number of HSCs. On the other hand, FGF2 can stimulate the proliferation of HSC without inhibition by the treatment period. It is suggested that GM-CSF and FGF2 may use different mechanisms to stimulate the HSCs proliferation. IP: 220.149.***.

저자
  • Minhee Kim(Division of Developmental Physiology, School of Biosciences and Chemistry, College of Natural Science, Sungshin Women's University)
  • Igjo Kang(Division of Developmental Physiology, School of Biosciences and Chemistry, College of Natural Science, Sungshin Women's University)
  • Yong-Pil Cheon(Division of Developmental Physiology, School of Biosciences and Chemistry, College of Natural Science, Sungshin Women's University)