AI Article Synopsis
- * Methods include using ELISA and flow cytometry to measure PDGF-BB and PDGFR-β levels, along with analyzing the activation of signaling pathways JAK2/STAT3 and PI3K/AKT in megakaryocytes.
- * Results indicate elevated PDGF-BB and PDGFR-β levels are linked to ET, affecting megakaryocyte production through specific pathways, and suggest that imatinib may provide a potential treatment by inhibiting PDGFR
Article Abstract
Objective: To 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.
Methods: The 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.
Results: The 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.
Conclusion: The 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.
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| http://dx.doi.org/10.7534/j.issn.1009-2137.2016.02.041 | DOI Listing |
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