| pubmed-article:2523262 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C0001271 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C0035696 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C1383860 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C1420192 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C1306673 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C0162788 | lld:lifeskim |
| pubmed-article:2523262 | lifeskim:mentions | umls-concept:C0027119 | lld:lifeskim |
| pubmed-article:2523262 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:2523262 | pubmed:dateCreated | 1989-6-2 | lld:pubmed |
| pubmed-article:2523262 | pubmed:abstractText | The development of cardiac hypertrophy secondary to pressure overload is accompanied by isoformic changes of contractile proteins such as myosin and actin. 35S-Labeled complementary RNA (cRNA) probes and in situ hybridization procedures were used for analysis of the regional distribution of newly formed transcripts from alpha-skeletal actin (alpha-sk-actin) and beta-myosin heavy chain (beta-MHC) genes during the early stages of pressure overload. The study was performed in 25-day-old rats submitted to a thoracic aortic stenosis and killed after surgery at times ranging from 4 hours to 3 days. Neither alpha-sk-actin nor beta-MHC messenger RNA (mRNA) was detected in the hearts of normal and sham-operated animals. However, alpha-sk-actin mRNA accumulated throughout the entire left ventricle as early as 4 hours after aortic stenosis, and by 12 hours was also detected in the left atrium. In contrast, beta-MHC mRNA was hardly detectable before day 1, and by days 2-3 was mainly restricted to the inner part of the left ventricle and around the coronary arteries. The absence of spatial and temporal coordination in the accumulation of alpha-sk-actin and beta-MHC mRNAs indicates that different signals and/or regulatory mechanisms are implicated in the induction of the two genes in response to hemodynamic overload. | lld:pubmed |
| pubmed-article:2523262 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2523262 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2523262 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2523262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2523262 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2523262 | pubmed:month | May | lld:pubmed |
| pubmed-article:2523262 | pubmed:issn | 0009-7330 | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:SchiaffinoSS | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:SchwartzKK | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:SamuelJ LJL | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:MarotteFF | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:RappaportLL | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:BuckinghamMM | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:SassoonDD | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:GarnerII | lld:pubmed |
| pubmed-article:2523262 | pubmed:author | pubmed-author:LompréA MAM | lld:pubmed |
| pubmed-article:2523262 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2523262 | pubmed:volume | 64 | lld:pubmed |
| pubmed-article:2523262 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2523262 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2523262 | pubmed:pagination | 937-48 | lld:pubmed |
| pubmed-article:2523262 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:2523262 | pubmed:meshHeading | pubmed-meshheading:2523262-... | lld:pubmed |
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| pubmed-article:2523262 | pubmed:meshHeading | pubmed-meshheading:2523262-... | lld:pubmed |
| pubmed-article:2523262 | pubmed:meshHeading | pubmed-meshheading:2523262-... | lld:pubmed |
| pubmed-article:2523262 | pubmed:meshHeading | pubmed-meshheading:2523262-... | lld:pubmed |
| pubmed-article:2523262 | pubmed:meshHeading | pubmed-meshheading:2523262-... | lld:pubmed |
| pubmed-article:2523262 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2523262 | pubmed:articleTitle | Nonsynchronous accumulation of alpha-skeletal actin and beta-myosin heavy chain mRNAs during early stages of pressure-overload--induced cardiac hypertrophy demonstrated by in situ hybridization. | lld:pubmed |
| pubmed-article:2523262 | pubmed:affiliation | INSERM U127, Université Paris VII, Hôpital Lariboisière, Paris, France. | lld:pubmed |
| pubmed-article:2523262 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2523262 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:2523262 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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