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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: Hypertension. 2021 May 24;78(1):230–240. doi: 10.1161/HYPERTENSIONAHA.121.17267

Figure 2. Rosiglitazone increases PPARγ activity and GCM1 mRNA expression while reducing sFLT1 secretion in the first trimester placenta.

Figure 2.

Treatment with Rosiglitazone caused a significant increase in PPARγ activity (p<0.05, n=3) (A). T0070907 did not cause a significant change in PPARγ activity (A). Rosiglitazone significantly upregulated PPARγ (p=0.0446, n=4) and GCM1 (p=0.0402, n=4) protein expression (B, C, F). T0070907 did not cause a significant change in PPARγ or GCM1 protein expression (B, C, F). Rosiglitazone significantly upregulated GCM1 mRNA expression (p=0.0433, n=4) (D). T0070907 significantly reduced GCM1 mRNA expression (p=0.02, n=4) (D). Rosiglitazone also caused a significant reduction in sFLT1 secretion (p=0.025, n=3) (E). Antagonizing PPARγ by T0070907 did not cause a statistically significant change in sFLT1 secretion (E). (Relative mRNA and protein expression were determine by normalization to housekeeping genes or protein. Relative expression values for individual tissue sets were normalized to DMSO (vehicle control, dotted line, set equal to 1) and subsequent statistical analysis was performed by student’s t-test to determine significant differences between groups,* p<0.05, ns=p>0.05, NT=not treated, Rosi=Rosiglitazone, T007=T0070907, bar plots and data reported are reported as mean ± SEM).