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However, its potential contribution to cardiovascular diseases remains to be assessed. Here, the roles of NOR<\/jats:styled-content>1 in cardiac hypertrophy induced by isoprenaline and the underlying molecular mechanisms were investigated.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>NOR<\/jats:styled-content>1 was expressed in cardiomyocytes treated with isoprenaline. After NOR<\/jats:styled-content>1 overexpression or knockdown in neonatal rat cardiomyocytes, cellular hypertrophy was monitored by measuring cell surface area and the mRNA<\/jats:styled-content> of hypertrophic biomarkers. Interactions between NOR<\/jats:styled-content>1 and PARP<\/jats:styled-content>\u20101 were investigated by co\u2010immunoprecipitation. NOR<\/jats:styled-content>1 expression and PARP<\/jats:styled-content>\u20101 activity were measured in rats with cardiac hypertrophy induced by isoprenaline.<\/jats:p><\/jats:sec>Key Results<\/jats:title>Treatment with isoprenaline significantly up\u2010regulated NOR<\/jats:styled-content>1 expression and PARP<\/jats:styled-content>\u20101 activity both in vivo<\/jats:italic> and in vitro<\/jats:italic>. Specific gene silencing of NOR<\/jats:styled-content>1 attenuated isoprenaline\u2010induced cardiomyocyte hypertrophy, whereas NOR<\/jats:styled-content>1 overexpression exacerbated cardiac hypertrophy. We identified a physical interaction between NOR<\/jats:styled-content>1 and PARP<\/jats:styled-content>\u20101, which was enhanced by NOR<\/jats:styled-content>1 transfection and thereby led to PARP<\/jats:styled-content>\u20101 activation. Overexpression of NOR<\/jats:styled-content>1, but not C293Y<\/jats:styled-content>, a NOR<\/jats:styled-content>1 mutant lacking the PARP<\/jats:styled-content>\u20101 binding activity, increased cellular surface area and the mRNA<\/jats:styled-content> levels of atrial natriuretic factor and brain natriuretic polypeptide, effects blocked by the PARP<\/jats:styled-content>\u20101 inhibitor 3\u2010aminobenzamide or siRNA<\/jats:styled-content> for PARP<\/jats:styled-content>\u20101.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>This is the first evidence that NOR<\/jats:styled-content>1 was involved in isoprenaline\u2010induced cardiac hypertrophy. The pro\u2010hypertrophic effect of NOR<\/jats:styled-content>1 can be partly attributed to its regulation of PARP<\/jats:styled-content>\u20101 enzymic activity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.13091","type":"journal-article","created":{"date-parts":[[2015,1,27]],"date-time":"2015-01-27T09:13:47Z","timestamp":1422350027000},"page":"2852-2863","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["The orphan receptor NOR<\/scp>1 participates in isoprenaline\u2010induced cardiac hypertrophy by regulating PARP<\/scp>\u20101"],"prefix":"10.1111","volume":"172","author":[{"given":"Xiao\u2010Jun","family":"Feng","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences Sun Yat\u2010Sen University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Gao","sequence":"additional","affiliation":[{"name":"Department 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