Activation of Janus kinase/signal transducers and activators of transcription pathway involved in megakaryocyte proliferation induced by vanadium resembles some aspects of essential thrombocythemia

Janus kinase 2 Thrombopoietin receptor Thrombopoiesis
DOI: 10.1177/0748233713518600 Publication Date: 2014-01-18T03:26:20Z
ABSTRACT
Vanadium (V) is an air pollutant released into the atmosphere by burning fossil fuels. Also, it has been recently evaluated for their carcinogenic potential to establish permissible limits of exposure at workplaces. We previously reported increase in number and size platelets precursor cells megakaryocytes bone marrow spleen. The aim this study was identify involvement Janus kinase/signal transducers activators transcription (JAK/STAT) pathway thrombopoietin (TPO) receptor, myeloproliferative leukemia virus oncogene (Mpl), megakaryocyte proliferation induced compound. Mice were exposed twice a week vanadium pentoxide inhalation (0.02 M) killed 4th, 6th, 8th exposure. Phosphorylated JAK2 (JAK2 ph), STAT3 (STAT3 STAT5, Mpl identified mice spleen cytofluorometry immunohistochemistry. An ph ph, but decrease 8-week our findings. Taking together, we propose that morphological findings, JAK/STAT activation, decreased receptor V leads condition comparable essential thrombocythemia, so effect on caused different mechanisms similar. also suggest negative feedback mechanism after activation. Since are platelet precursors, alteration affects morphology function, which might have implications hemostasis as demonstrated previously, important continue evaluating effects toxics pollutants platelets.
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