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Both the Arctic and Antarctic sea ice extents (SIEs) from 44 coupled models in the Coupled Model Intercomparison Project Phase 6 (CMIP6) are evaluated by comparing them with observations and CMIP5 results. The CMIP6 multimodel mean can adequately reproduce the seasonal cycles of both the Arctic and Antarctic SIE. The observed Arctic September SIE declining trend (−0.82 ± 0.18 million km 2 per decade) between 1979 and 2014 is slightly underestimated in CMIP6 models (−0.70 ± 0.06 million km 2 per decade). The observed weak but significant upward trend of the Antarctic SIE is not captured, which was an issue already in the CMIP5 phase. Compared with CMIP5 models, CMIP6 models have lower intermodel spreads in SIE mean values and trends, although their SIE biases are relatively larger. The CMIP6 models did not reproduce the new summer tendencies after 2000, including the faster decline of Arctic SIE and the larger interannual variability in Antarctic SIE.

Membrane-associated prostaglandin (PG) E 2 synthase-1 (mPGES-1) catalyzes the conversion of PGH 2 to PGE 2 , which contributes to many biological processes. Peroxisome proliferator-activated receptor ␥ (PPAR␥) is a ligand-activated transcription factor and plays an important role in growth, differentiation, and inflammation in different tissues. Here, we examined the effect of PPAR␥ ligands on interleukin-1␤ (IL-1␤)-induced mPGES-1 expression in human synovial fibroblasts. PPAR␥ ligands 15-deoxy-⌬ 12,14 prostaglandin J 2 (15d-PGJ 2 ) and the thiazolidinedione troglitazone (TRO), but not PPAR␣ ligand Wy14643, dose-dependently suppressed IL-1␤-induced PGE 2 production, as well as mPGES-1 protein and mRNA expression. 15d-PGJ 2 and TRO suppressed IL-1␤-induced activation of the mPGES-1 promoter. Overexpression of wild-type PPAR␥ further enhanced, whereas overexpression of a dominant negative PPAR␥ alleviated, the suppressive effect of both PPAR␥ ligands. Furthermore, pretreatment with an antagonist of PPAR␥, GW9662, relieves the suppressive effect of PPAR␥ ligands on mPGES-1 protein expression, suggesting that the inhibition of mPGES-1 expression is mediated by PPAR␥. We demonstrated that PPAR␥ ligands suppressed Egr-1-mediated induction of the activities of the mPGES-1 promoter and of a synthetic reporter construct containing three tandem repeats of an Egr-1 binding site. The suppressive effect of PPAR␥ ligands was enhanced in the presence of a PPAR␥ expression plasmid. Electrophoretic mobility shift and supershift assays for Egr-1 binding sites in the mPGES-1 promoter showed that both 15d-PGJ 2 and TRO suppressed IL-1␤-induced DNA-binding activity of Egr-1. These data define mPGES-1 and Egr-1 as novel targets of PPAR␥ and suggest that inhibition of mPGES-1 gene transcription may be one of the mechanisms by which PPAR␥ regulates inflammatory responses.