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. 2016 Sep 9;311(5):L855–L867. doi: 10.1152/ajplung.00272.2016

Fig. 6.

Fig. 6.

PPARγ ligand production by IL-1β-activated HLFs is dependent on COX-2 and lipocalin-type PGD synthase (L-PGDS), but not microsomal PGE synthase (mPGES-1) or hematopoietic PGDS (H-PDGS). Primary HLFs were treated for 72 h with 0.1 ng/ml IL-1β + vehicle (0.1% DMSO) or 1 of 3 selective COX-2 inhibitors (COX-2i), celecoxib (Cel) at 1 μM, SC-58125 at 1 μM, or NS-398 at 10 μM; the L-PGDS inhibitor (L-PGDSi) AT-56 at 100 μM; or the H-PGDS inhibitor (H-PGDSi) HQL-79 at 25 μM (A) or the mPGES-1 inhibitor (mPGESi) arzanol (Arz) at 0.5–2.5 μM (B). Conditioned medium was then harvested and tested for PPARγ ligand content using a PPRE-luciferase reporter (A and B) or PGE2 content was determined by EIA (C). Values are means ± SD of 3–6 independent biological replicates per condition. *P < 0.05, ***P < 0.001 vs. vehicle alone; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. IL-1β + vehicle (by unpaired t-test).