Figure 4.
Effects of peroxisome-proliferator-activated receptor β/δ (PPARβ/δ) agonist (GW), hormones (H), and MEK inhibitor (PD) were assessed. A, Time-course and additive effects of GW + H for up to 72 hours were observed for endometrial stromal cell (ESC) expression of estrogen receptor α (ERα) (panel 1), PR-A and -B (panel 2), nonphospho-connexin 43 (Cx43) Ser368 (panel 4), and phospho-Cx43 Ser368 (panel 3). β-Actin levels (panel 5) are shown. Lane 1 represents untreated control cells. B, Relative to controls, a combination of GW, H, and PD for 72 hours led to the lowest phospho-extracellularly regulated kinase (ERK)1/2 (panel 1), phospho-p90 RSK (panel 2), phospho-p70/85 S6Kinase (panel 3) and was associated with the highest levels of total Cx43 (panel 4) and PR-A and -B (panel 5) (P < .05, t-test, n = 3). β-Actin levels (panel 6) are shown as loading controls.

Effects of peroxisome-proliferator-activated receptor β/δ (PPARβ/δ) agonist (GW), hormones (H), and MEK inhibitor (PD) were assessed. A, Time-course and additive effects of GW + H for up to 72 hours were observed for endometrial stromal cell (ESC) expression of estrogen receptor α (ERα) (panel 1), PR-A and -B (panel 2), nonphospho-connexin 43 (Cx43) Ser368 (panel 4), and phospho-Cx43 Ser368 (panel 3). β-Actin levels (panel 5) are shown. Lane 1 represents untreated control cells. B, Relative to controls, a combination of GW, H, and PD for 72 hours led to the lowest phospho-extracellularly regulated kinase (ERK)1/2 (panel 1), phospho-p90 RSK (panel 2), phospho-p70/85 S6Kinase (panel 3) and was associated with the highest levels of total Cx43 (panel 4) and PR-A and -B (panel 5) (P < .05, t-test, n = 3). β-Actin levels (panel 6) are shown as loading controls.

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