Inhibition of Histone Deacetylase Activity Diminishes Pressure Overloaded Cardiac Hypertrophy in Mice
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서지정보
ㆍ발행기관 : 한국동물번식학회
ㆍ수록지정보 : Reproductive & developmental biology / 35권 / 2호
ㆍ저자명 : Yunkyung Hong, Jongwook Song, Sang-Kil Lee, Youngjeon Lee, Gyu-Jin Rho, Joo-Heon Kim, Yonggeun Hong
ㆍ저자명 : Yunkyung Hong, Jongwook Song, Sang-Kil Lee, Youngjeon Lee, Gyu-Jin Rho, Joo-Heon Kim, Yonggeun Hong
목차
ABSTRACT INTRODUCTION MATERIALS AND METHODS Materials Animal Surgery Histological Staining Immunoblot Analysis Statistical Analysis RESULTS TSA Diminishes the TAB-Induced Cardiac Hypertrophy HDAC Suppression by TSA Leads to Dose-Responsive Blunted of Pathologic Cardiac Growth Immunoblot Analysis on Histone Acetylation Duration of Histone H3 Activity by TSA in H9c2 Cells DISCUSSION REFERENCES영어 초록
To explore the role of histone deactylase (HDAC) activation in an in vivo model of hypertrophy, we studied the effects of Trichostatin A (TSA). TSA subjected to thoracic aortic banding (TAB)-induced pressure stress in mice. In histological observations, TAB in treated mice showed a significant hypertrophic response, whereas the sham operation remained nearly normal structure with partially blunted hypertrophy. TSA treatment had no effect (measured as HW/BW) on sham-operated animals. TAB animals treated with vehicle manifested a robust ~50% hypertrophic response (p<0.05 vs sham). TAB mice treated with 2 mg/kg/day TSA manifested a blunted growth responses, which was significantly diminished (p<0.05) compared with vehicle-treated TAB mice. TAB mice treated with a lower dose of TSA (0.5 mg/kg/day) manifested a similar blunting of hypertrophic growth (~25% increase in heart mass). Furthermore, to determine activity duration of TSA in vitro, 1 nM TSA was added to H9c2 cells. Histone acetylation was initiated at 4 hr after treatment, and it was peak up to 18 hr, then followed by significantly reduced to 30 hr. We also analyzed the expression of p53 following TSA treatment, wherein p53 expression was elevated at 4 hr, and it was maintained to 24 hr after treatment. ERK was activated at 8 hr, and maintained till 30 hr after treatment suggesting an intracellular signaling interaction between TSA and p53 expression. Taken together, it is suggested that HDAC activation is required for pressure-overload growth of the heart. Eventually, these data suggest that histone acetylation may be a novel target for therapeutic intervention in pressure-overloaded cardiac hypertrophy.참고 자료
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