Author + information
- Chengzhang Xu1,
- Jingfeng Wang1,
- Shaohua Wang1,
- Wenhao Liu1,
- Yongqing Lin1,
- Haifeng Zhang1 and
- Yangxin Chen1
Cardiac-specific PPAR-γ overexpression in mice lead to susceptible to sudden death. Connexin 43 (Cx43) plays an important role in arrhythmia and sudden death. To directly assess alterations of Cx43 and microRNA-1 (miR-1) and miR-206, which are muscle-specific miRs and regulation Cx43 expression, in the heart of PPAR-γ overexpression mice.
Relative young (3 weeks) transgenetic cardiac-specific PPAR-γ(MHC-PPAR-γ) overexpression mice with low (PPAR-γ L) and high (PPAR-γ H) levels, and control mice were used. Heart weight (HW), body weight (BW), HW/BW ratio, and serum brain natriuretic peptide (BNP) were recorded. Cx43 expressions were measured by RT-PCR and western blot and miRs abundance were assayed using real-time quantitative RT-PCR (qRT-PCR).
Cx43 contents, both in mRNA and protein levels, in heart with PPAR-γ H were significantly lower than those with PPAR-γ L and control heart. Moreover, Cx43 mRNA levels tended to be negatively correlated to MHC-PPAR-γ (r = -0.38; P<0.01) in PPAR-γ H mice. miR-1 level was higher in PPAR-γ H mice. miR-206 also tended to be increased in PPAR-γ H mice but did not reach statistical significance. miR-1 level was positively correlated to MHC-PPAR-γ (r = 0.38; P = 0.02) in PPAR-γ H mice. miR-1 level was negatively correlated to Cx43 mRNA abundance (r = -0.36; P<0.01).
Cardiac-specific overexpression of PPAR-γ leads to a reduction of Cx43 in the heart, which may be mediated by the increased miR-1 contents.