| First Author | Misaka T | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 439 |
| Issue | 1 | Pages | 142-7 |
| PubMed ID | 23933320 | Mgi Jnum | J:211379 |
| Mgi Id | MGI:5574565 | Doi | 10.1016/j.bbrc.2013.08.002 |
| Citation | Misaka T, et al. (2013) Senescence marker protein 30 inhibits angiotensin II-induced cardiac hypertrophy and diastolic dysfunction. Biochem Biophys Res Commun 439(1):142-7 |
| abstractText | BACKGROUND AND OBJECTIVE: Senescence marker protein 30 (SMP30) is assumed to behave as an anti-aging factor. Recently, we have demonstrated that deficiency of SMP30 exacerbates angiotensin II-induced cardiac hypertrophy, dysfunction and remodeling, suggesting that SMP30 may have a protective role in the heart. Thus, this study aimed to test the hypothesis that up-regulation of SMP30 inhibits cardiac adverse remodeling in response to angiotensin II. METHODS: We generated transgenic mice with cardiac-specific overexpression of SMP30 gene using alpha-myosin heavy chain promoter. Transgenic mice and wild-type littermate mice were subjected to continuous angiotensin II infusion (800 ng/kg/min). RESULTS: After 14 days, heart weight and left ventricular weight were lower in transgenic mice than in wild-type mice, although blood pressure was similarly elevated during angiotensin II infusion. Cardiac hypertrophy and diastolic dysfunction in response to angiotensin II were prevented in transgenic mice compared with wild-type mice. The degree of cardiac fibrosis by angiotensin II was lower in transgenic mice than in wild-type mice. Angiotensin II-induced generation of superoxide and subsequent cellular senescence were attenuated in transgenic mouse hearts compared with wild-type mice. CONCLUSIONS: Cardiac-specific overexpression of SMP30 inhibited angiotensin II-induced cardiac adverse remodeling. SMP30 has a cardio-protective role with anti-oxidative and anti-aging effects and could be a novel therapeutic target to prevent cardiac hypertrophy and remodeling due to hypertension. |
