Title : Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2.

Pub. Date : 2021 Apr 21

PMID : 33919366






6 Functional Relationships(s)
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Protein Name
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1 Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2. Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens
2 The current study addressed the question of how palmitate might interact with insulin or PGE2 to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens
3 The current study addressed the question of how palmitate might interact with insulin or PGE2 to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens
4 PGE2 in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens
5 PGE2 in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens
6 Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE2 in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle. Dinoprostone C-X-C motif chemokine ligand 8 Homo sapiens