Figure 4
From: Expression of the Hutchinson-Gilford Progeria Mutation Leads to Aberrant Dentin Formation
Defects in signaling pathways and downregulation of matrix protein expression in progerin-expressing odontoblasts. (a) Promoter activities for BMP and TGFβ signaling were analyzed and compared in MDPC-23 transfected with Δ50 lamin A, WT lamin A and the negative control by luciferase reporters of BRE and SBE, respectively. (b) Promoter activities for Wnt/β-catenin signaling were analyzed and compared in MDPC-23 transfected with Δ50 lamin A, WT lamin A and the negative control by luciferase reporters of FOPflash/TOPflash. (c) Western blot of cytoplasmic and nuclear protein was performed using antibodies for nonphosphor-β-catenin (Active β-Cat), β-catenin (β-Cat), histone H3 and α-tubulin. Progerin expression by transfection of G608G lamin A and Δ50 lamin A impairs nuclear translocation of β-catenin. The samples shown were derived from the same experiment, and all gels/blots were processed under the same experimental conditions. α-tubulin and histone H3 were used as a loading control for cytoplasmic and nuclear protein, respectively. Cropped images are displayed here; the original full-size blots are presented in Supplementary Fig. S6. (d) The transcript levels of dentin matrix-related genes in MDPC-23 transfected with Δ50 lamin A, WT lamin A and the negative control were analyzed and compared by real-time qPCR. Significance was assigned for p-values as indicated.
