PubMed:14975762 JSONTXT

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":92,"end":97},"obj":"HP_0002664"},{"id":"T2","span":{"begin":1089,"end":1102},"obj":"HP_0001635"}],"text":"Expression of p300 protects cardiac myocytes from apoptosis in vivo.\nDoxorubicin is an anti-tumor agent that represses cardiac-specific gene expression and induces myocardial cell apoptosis. Doxorubicin depletes cardiac p300, a transcriptional coactivator that is required for the maintenance of the differentiated phenotype of cardiac myocytes. However, the role of p300 in protection against doxorubicin-induced apoptosis is unknown. Transgenic mice overexpressing p300 in the heart and wild-type mice were subjected to doxorubicin treatment. Compared with wild-type mice, transgenic mice exhibited higher survival rate as well as more preserved left ventricular function and cardiac expression of alpha-sarcomeric actin. Doxorubicin induced myocardial cell apoptosis in wild-type mice but not in transgenic mice. Expression of p300 increased the cardiac level of bcl-2 and mdm-2, but not that of p53 or other members of the bcl-2 family. These findings demonstrate that overexpression of p300 protects cardiac myocytes from doxorubicin-induced apoptosis and reduces the extent of acute heart failure in adult mice in vivo."}

{"project":"bc5cdr-valid-experiment","denotations":[{"id":"T1","span":{"begin":69,"end":80},"obj":"Chemical"},{"id":"T2","span":{"begin":92,"end":97},"obj":"Disease"},{"id":"T3","span":{"begin":191,"end":202},"obj":"Chemical"},{"id":"T4","span":{"begin":394,"end":405},"obj":"Chemical"},{"id":"T5","span":{"begin":522,"end":533},"obj":"Chemical"},{"id":"T6","span":{"begin":724,"end":735},"obj":"Chemical"},{"id":"T7","span":{"begin":1027,"end":1038},"obj":"Chemical"},{"id":"T8","span":{"begin":1089,"end":1102},"obj":"Disease"}],"text":"Expression of p300 protects cardiac myocytes from apoptosis in vivo.\nDoxorubicin is an anti-tumor agent that represses cardiac-specific gene expression and induces myocardial cell apoptosis. Doxorubicin depletes cardiac p300, a transcriptional coactivator that is required for the maintenance of the differentiated phenotype of cardiac myocytes. However, the role of p300 in protection against doxorubicin-induced apoptosis is unknown. Transgenic mice overexpressing p300 in the heart and wild-type mice were subjected to doxorubicin treatment. Compared with wild-type mice, transgenic mice exhibited higher survival rate as well as more preserved left ventricular function and cardiac expression of alpha-sarcomeric actin. Doxorubicin induced myocardial cell apoptosis in wild-type mice but not in transgenic mice. Expression of p300 increased the cardiac level of bcl-2 and mdm-2, but not that of p53 or other members of the bcl-2 family. These findings demonstrate that overexpression of p300 protects cardiac myocytes from doxorubicin-induced apoptosis and reduces the extent of acute heart failure in adult mice in vivo."}