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. Author manuscript; available in PMC: 2010 Oct 22.
Published in final edited form as: Cell. 2007 Aug 10;130(3):427–439. doi: 10.1016/j.cell.2007.06.044

Figure 6. G6PD Deficiency Prevents Cardiac Hypertrophy and Protein Aggregation in hR120GCryAB High mice in vivo.

Figure 6

(A) G6PD activity in heart homogenates of hR12GCryAB High Tg/G6PDmut is similar to NTg and significantly lower than hR12GCryAB High Tg at 6 months (p<0.01).

(B) Cardiac hypertrophy (assessed by heart weight/body weight ratio) caused by hR120GCryAB Tg overexpression was completely prevented by G6PD deficiency in R12GCryAB High Tg/G6PDmut hearts. HW=heart weight. BW=body weight.

(C, D) Protein abundance of total CryAB, Hsp25, G6PD, and MnSOD in hR120GCryAB High Tg and hR120GCryAB High Tg/G6PDmut hearts. Each lane in panel C represents an individual animal per experimental group (3 animals/group). (*p<0.05, † p<0.015, **p<0.001). Lane 13 is blank in the G6PD and Hsp25 panels.

(E) G6PD deficiency prevents protein aggregation in hR120GCryAB High Tg expression crossed into G6PDmut animals. Arrows in panel (a) point to examples of the large protein aggregates (green, CryAB; red, Hsp25; and blue, G6PD), which are not found in the transgenic hR120GCryAB High Tg/G6PDmut mice (b).