- Author:
Li-Xia ZHOU
1
;
En-Yu LIANG
1
;
Jie-Yu YE
2
;
Mo YANG
3
Author Information
- Publication Type:Journal Article
- MeSH: Bone Marrow; metabolism; Case-Control Studies; Humans; Megakaryocytes; metabolism; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-sis; metabolism; Receptor, Platelet-Derived Growth Factor beta; metabolism; Signal Transduction; Thrombocythemia, Essential; metabolism; Thrombopoiesis
- From: Journal of Experimental Hematology 2016;24(2):526-530
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the role of PDGF/PDGFR in essential thrombocythemia (ET) by investigating the expression of PDGF-BB in bone marrow and the expression of PDGFR-β in bone marrow cells of patients with ET and explore the new target for treating ET patients through inhibiting the PDGFR of megakaryocytes.
METHODSThe expression level of PDGF-BB in bone marrow of ET patients and normal controls were assayed by using ELISA, the expression level of PDGFR-β (CD140) in bone marrow of ET patients and normal controls were detected by using flow cytometry, the effect of PDGF-BB in JAK2/STAT3 and PI3K/AKT pathway was detected by using flow cytometry or Werstern blot, and the effect of imatinib on the megakaryopoiesis of PDGF was observed.
RESULTSThe expression level of PDGF-BB in bone marrow of ET patients was significantly higher than that in normal controls; the expression level of PDGFR-β in bone marrow of ET patients was significantly higher than that in nornal controls; PDGF-BB could activate JAK2/STAT3 and PI3K/AKT pathway of megakaryocytes, while the imatinib could block the effect of PDGF-BB on megakaryocyte.
CONCLUSIONThe elevated PDGF-BB and PDGFR-β may be involved in ET, and the physiopathologic mechanism is that the elevated PDGF-BB activates PDGFR with subsequent activation of the JAK2/STAT3 and PI3K/AKT pathways, stimulating megakaryopoiesis. Imatinib may have a therapeutical effect on ET via blocking of PDGFR.