Supplementary information
From the following article:
Anti-inflammatory lipid mediators and insights into the resolution of inflammation
Toby Lawrence, Derek A. Willoughby & Derek W. Gilroy
Nature Reviews Immunology 2, 787-795 (October 2002)
doi:10.1038/nri915
Online figure 1| Biochemical pathway for arachidonic-acid release and eicosanoid biosynthesis. Arachidonic acid is liberated through the action of phospholipase enzymes, and converted to prostaglandin G2 (PGG2) and, subsequently, PGH2 by cyclooxygenase. Specific synthase enzymes then generate the different classes of prostaglandin. PLA2, phospholipase A2 (c, cytosolic; i, Ca2+ independent; s, secretory); hPGD2S, prostaglandin D2 synthase; mPGE2S/cPGE2S, prostaglandin E2 synthase; TxA2, thromboxane A2.
Online figure 2| Biochemical pathway for lipoxin biosynthesis. The sequential action of 12- or 15-lipoxygenase (LO) and specific lipoxin hydrolase enzymes generates lipoxin A4 (LXA4) and LXB4 from leukotriene A4 (LTA4).
Online figure 3| Cyclopentenone-prostaglandin formation. Prostaglandin D2 (PGD2), PGE2 and PGE1 are spontaneously metabolized to the cyclopentenone derivatives PGJ2, PGA2 and PGA1, respectively, by dehydrogenation. These cyclopentenone prostaglandins share the structural feature of a reactive carbonyl group in the cyclopentane ring.
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