Phosphatidylserine (PS), which is normally located on the inner leaflet of the plasma membrane, translocates to the outer leaflet during early stages of apoptosis,. The externalization of PS provides a signal for phagocytes to initiate uptake of apoptotic cells. After the phagocytosis of apoptotic cells, phagocytes start to secrete anti-inflammatory mediators including prostaglandin E2 (PGE2), which act an autocrine manner to control their functions. PS-containing liposomes (PS liposomes) can mimic the effects of apoptotic cells on phagocytes to induce the secretion of PGE2. PS liposomes induced PGE2 secretion from microglia without induction of either cyclooxygenase (COX)-2 or microsomal prostaglandin E synthase (mPGES)-1. PS liposomes were found to utilize the COX-1/mPGES-2 system to produce PGE2 secretion and then shift microglia and macrophages from a pro- to anti-inflammatory phenotype by the autocrine action of PGE2. Moreover, PS liposomes inhibit the maturation of dendritic cells and osteoclast precursors. Therefore, PS liposomes may be potentially useful as one type of pharmacological intervention for inflammatory and immune diseases through a feedback mechanism involving PGE2.
|Title of host publication||Prostaglandins|
|Subtitle of host publication||Biochemistry, Functions, Types and Roles|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||12|
|Publication status||Published - Jan 1 2011|
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)