Title : Elevated prostaglandin E2 post-bone marrow transplant mediates interleukin-1β-related lung injury.

Pub. Date : 2018 Mar

PMID : 28589946






4 Functional Relationships(s)
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1 Using a murine bone marrow transplant (BMT) model, we show that overexpression of prostaglandin E2 (PGE2) post-BMT signals via EP2 or EP4 to induce cyclic adenosine monophosphate (cAMP), which activates protein kinase A or the exchange protein activated by cAMP (Epac) to induce cAMP response element binding-dependent transcription of IL-1beta leading to exacerbated lung injury in BMT mice. Dinoprostone interleukin 1 beta Mus musculus
2 Using a murine bone marrow transplant (BMT) model, we show that overexpression of prostaglandin E2 (PGE2) post-BMT signals via EP2 or EP4 to induce cyclic adenosine monophosphate (cAMP), which activates protein kinase A or the exchange protein activated by cAMP (Epac) to induce cAMP response element binding-dependent transcription of IL-1beta leading to exacerbated lung injury in BMT mice. Dinoprostone interleukin 1 beta Mus musculus
3 Induction of IL-1beta by PGE2 is time and dose dependent. Dinoprostone interleukin 1 beta Mus musculus
4 Reducing PGE2 levels with indomethacin improved bacterial clearance and reduced IL-1beta-mediated acute lung injury in P. aeruginosa-infected BMT mice. Dinoprostone interleukin 1 beta Mus musculus