| pubmed-article:12193565 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0215825 | lld:lifeskim |
| pubmed-article:12193565 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:12193565 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:12193565 | pubmed:dateCreated | 2002-8-23 | lld:pubmed |
| pubmed-article:12193565 | pubmed:abstractText | We previously reported that adrenomedullin produced by cardiac myocytes acts as a local modulator in some cardiac disorders. However, the role of adrenomedullin (AM) in cardiomyocyte apoptosis remains to be clarified. The present study investigated the effect of AM on doxorubicin-induced cardiac myocyte apoptosis. Doxorubicin increased the number of cells with pyknotic nuclei and lactate dehydrogenase release, and AM dose-dependently (10(-10)-10(-8)6 M) inhibited these increases produced by doxorubicin. Treatment with AM also suppressed doxorubicin-induced DNA fragmentation and caspase-3 activation. 8-Bromo-cAMP, a cAMP analog, mimicked these antiapoptotic effects of AM. An AM/calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37) and a protein kinase A inhibitor H89 attenuated the antiapoptotic effect of AM. CGRP-(8-37) and H89 had no apoptotic effect alone, but accelerated doxorubicin-induced apoptosis. Under serum-free conditions, AM secretion into the culture medium and expression of AM mRNA were significantly increased after treatment with doxorubicin. Hydrogen peroxide scavenger catalase and antioxidant N-acetyl-L-cysteine inhibited the doxorubicin-mediated increase in AM secretion and its gene expression. These results indicate that AM inhibits doxorubicin-induced cardiac myocyte apoptosis through a cAMP-dependent mechanism and suggest that augmented production of AM by doxorubicin has an endogenous antiapoptotic effect. AM, as an autocrine factor, may play a protective role against cardiomyocyte injury by doxorubicin. | lld:pubmed |
| pubmed-article:12193565 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12193565 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12193565 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12193565 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12193565 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:KangawaKenjiK | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:YoshiharaFumi... | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:HorioTakeshiT | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:KawanoYuheiY | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:SugaShin-Ichi... | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:KohnoMasakazu... | lld:pubmed |
| pubmed-article:12193565 | pubmed:author | pubmed-author:TokudomeTakes... | lld:pubmed |
| pubmed-article:12193565 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12193565 | pubmed:volume | 143 | lld:pubmed |
| pubmed-article:12193565 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12193565 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12193565 | pubmed:pagination | 3515-21 | lld:pubmed |
| pubmed-article:12193565 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:12193565 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12193565 | pubmed:articleTitle | Adrenomedullin inhibits doxorubicin-induced cultured rat cardiac myocyte apoptosis via a cAMP-dependent mechanism. | lld:pubmed |
| pubmed-article:12193565 | pubmed:affiliation | Research Institute, National Cardiovascular Center, Suita, Osaka 565-8565, Japan. | lld:pubmed |
| pubmed-article:12193565 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12193565 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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