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- W4313374516 abstract "Abstract The JAK2V617F mutation is intimately involved in the pathogenesis of myeloproliferative neoplasms (MPNs) including polycythemia vera and essential thrombocytosis. The thrombotic events are serious complications occurring in individuals with MPNs which affect their prognosis. Interestingly, JAK2V617F is detected in some individuals who developed thrombosis without MPNs and thrombotic risk factors. These observations prompted us to hypothesize that JAK2V617F arising in myeloid cells could contribute to cardiovascular disease by promoting the production of proinflammatory cytokines. To test this, we established JAK2V617F expressing murine macrophages (JAK2V617F macrophages) and explored their function. We found that the levels of p-STAT3, one of downstream targets of JAK2, were markedly elevated in JAK2V617F macrophages in associated with an increase in the production of IL-6 at baseline and following stimulation with LPS, as measured by Western blotting and ELISA, respectively. While, inhibition of STAT3 by C188-9 significantly decreased the production of IL-6 in the culture medium harvested from JAK2V617F macrophages. In further experiments, JAK2V617F endowed macrophages with elevated glycolytic phenotype in parallel with aberrant expression of PKM1. Interestingly, silencing of PKM1 inactivated STAT3. On contrary, ectopic expression of PKM1 activated STAT3. Importantly, JAK2V617F contributed to PKM1 protein stabilization via blockade of lysosomal-dependent degradation via chaperone-mediated autophagy (CMA). All of these observations indicated that JAK2V617F could protect PKM1 from CMA-mediated degradation, leading to activation of STAT3, which promoted IL-6 production." @default.
- W4313374516 created "2023-01-06" @default.
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- W4313374516 date "2020-05-01" @default.
- W4313374516 modified "2023-09-23" @default.
- W4313374516 title "JAK2V617F expressing macrophages stimulate IL-6 production through PKM1 mediated STAT3 activation" @default.
- W4313374516 doi "https://doi.org/10.4049/jimmunol.204.supp.59.18" @default.
- W4313374516 hasPublicationYear "2020" @default.
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