Quantitative analysis of growth factor production in the mechanism of fibrosis in agnogenic myeloid metaplasia.

作者: Jen C. Wang , Tsong H. Chang , Amit Goldberg , Allan D. Novetsky , Steve Lichter

DOI: 10.1016/J.EXPHEM.2006.07.004

关键词: MyelofibrosisGrowth factorPlatelet-derived growth factor receptorInternal medicineBiologyTransforming growth factorFibroblast growth factorFibrosisCD34EndocrinologyCD14

摘要: Objective The current study quantified the growth factors in megakaryocytes and monocytes correlated them to degree of fibrosis, as there is no quantitative analysis from or reported patients with agnogenic myeloid metaplasia (AMM). Materials Methods Megakaryocytes were obtained cultured blood CD34 + cells. CD14 cells sorted by magnetic cell sorting. Quantitative analyses real-time reverse-transcriptase polymerase chain reaction techniques enzyme-linked immunobsorbent assay (ELISA). Results 1) We found that mRNA levels transforming factor (TGF) β1, platelet-derived (PDGF), fibroblast (FGF) produced significantly elevated AMM compared those normal controls ( p not other MPDs controls; only some patients. 4) correlation these myelofibrosis was significant r = 0.73) but 0.23). 5) ELISA showed most MPDs, volunteer controls, undetectable, a few (three each TGF-β1 PDGF one FGF) (two had protein factors. Conclusions In AMM, fibrosing are megakaryocytes, they monocyte-macrophage lineages. 2) more abundantly than FGF megakaryocytes. 3) A statistically between suggests may be associated etiology bone marrow fibrosis AMM. Failure substantiate at level main source production initiating translation also important process Further studies necessary.

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