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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Hypertension. 2016 Jan 18;67(3):597–605. doi: 10.1161/HYPERTENSIONAHA.115.06412

Figure 6. Cardiac specific overexpression of Rnd3 protected the heart from the transition to heart failure by preserving responsive angiogenesis.

Figure 6

(a) Representative Rnd3 protein expression levels in the hearts of WT and Rnd3 transgenic (MHC-Rnd3) mice by Western blot analysis. (b) MHC-Rnd3 mice have reserved cardiac function and developed less severe heart failure after TAC. Only slight decreases in the cardiac ejection fractions and fractional shortenings were detected in MHC-Rnd3 mice after TAC compared to WT mice from the Sham group. (c) No significant increase in the LVID in systole was detected by echocardiography in MHC-Rnd3 mice after TAC compared to the Sham WT mice. (d) MHC-Rnd3 mice have preserved capillary function after TAC compared to WT mice. (e) More capillaries were observed in the post-TAC MHC-Rnd3 mouse heart by isolectin staining (green). (f) Larger capillary areas and more capillary numbers were observed in the MHC-Rnd3 mouse heart compared to the WT control after TAC. Cardiac capillaries were quantified by LAS V4.0 software (Germany). The numbers in the columns represented the number of mice in each group.