Research Paper Volume 13, Issue 1 pp 493—515

Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway

Adenoviral overexpression of MICU1 was resistant to cardiomyocyte hypertrophy in vitro. (A, B) Representative immunoblots and quantification of protein levels of MICU1 in (NMVMs) (A) and Ang-II treated NMVMs (B) infected with Ad-EV and Ad-MICU1 were shown. (C, D) Cell surface areas were measured in NMVMs stimulated with Ang-II (C) and representative images of α-actinin (red)-and DAPI (blue)-stained cardiomyocytes (left) were followed by cell area quantifications (D). Scale bars=10 μm. (E–H) Western blotting and qRT-PCR were used to measure protein levels of ANP, BNP and β-MHC in NMVMs and Ang-II treated NMVMs. All the data represent the means ± SEM. N=6-8/group. **P##P&&PΨΨP

Figure 5. Adenoviral overexpression of MICU1 was resistant to cardiomyocyte hypertrophy in vitro. (A, B) Representative immunoblots and quantification of protein levels of MICU1 in (NMVMs) (A) and Ang-II treated NMVMs (B) infected with Ad-EV and Ad-MICU1 were shown. (C, D) Cell surface areas were measured in NMVMs stimulated with Ang-II (C) and representative images of α-actinin (red)-and DAPI (blue)-stained cardiomyocytes (left) were followed by cell area quantifications (D). Scale bars=10 μm. (EH) Western blotting and qRT-PCR were used to measure protein levels of ANP, BNP and β-MHC in NMVMs and Ang-II treated NMVMs. All the data represent the means ± SEM. N=6-8/group. **P<0.01 vs. Vehicle in Normal; ##P<0.01 vs. Vehicle in Ang-II; &&P<0.01 vs. Normal; ΨΨP<0.01 vs. Ad-EV of Ang-II.