I have just started to work with THP-1 monocytes, but cannot seem to find information on the mechanism of PMA on THP-1 for differentiating them into macrophages. Does anyone know what the mechanism is or can suggest some papers to find answers.
Following the paradigm of differentiation in PC12 cells I would suggest that this happens via ERK, PMID:7835430
Cheers. I will check out the paper. I look forward to your talk at the ICSA conference in Spain.
Dominick, PMA is a real strong inducer of protein kinase C, and via that, induces a lot of other kinases. It can work MEK independent, but still leads to activation of ERK1/2. It also is an endogenous inducer of superoxide, and via this, induces a lot of feedback mechanisms. Through all these pathways, it subsequently leads to stimulation of NFkB and AP-1 transcription factors. Hope this helps.
Hi Dominic, do you have any idea which concentration of Phorbol you normally use to activate the cells? I am trying to activate chicken HD 11 cells (macrophages) with 100 ng/ml for 12 hours. It activates for sure. But I realized that with this there are lot of dead cells (60%) .
Dinesh
Dear team, I used PMA to induce superoxide production in salmon primary leucocytes. I observed the highest peak just after 30 min and a second peak 12 hrs later. What could explain this bimodal behavior of superoxide production in leucocytes induced with PMA?. I would also like to be highlighted on what causes cells to aggregate following treatment with PMA?
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