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. 2013 May 7;12:38. doi: 10.1186/1476-4598-12-38

Figure 2.

Figure 2

16E5 is responsible for TGFβRII mRNA down-modulation. A) HaCaT pMSG E5 were treated with dexamethasone for different times (6 h, 12 h, 24 h). HaCaT pMSG were used as negative control. The 16E5 (left panel) and TGFβRII (right panel) transcript levels were estimated by real-time RT-PCR. Results are expressed as mean values ± standard deviation (SD). Student’s t test was performed as reported above NS vs HaCaT pMSG -Dex, *p < 0.001 vs HaCaT pMSG E5 cells -Dex, **p < 0.001 vs HaCaT pMSG E5 cells + Dex 6 h, ***p < 0.05 vs HaCaT pMSG E5 cells + Dex 6 h, B) HaCaT cells were transiently transfected with increasing amounts of pCI-neo E5-HA expression vector (0.5 μg, 1 μg and 2 μg) (HaCaT E5) or using the empty vector alone (HaCaT pCI-neo). After transfection, the 16E5 mRNA (left panel) and TGFβRII mRNA (right panel) were quantified by real-time RT-PCR. *p < 0.001 vs HaCaT E5 cells (0.5 μg cDNA), **p < 0.005 vs HaCaT E5 cells (1 μg cDNA).