File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1161/01.RES.63.2.448
- Scopus: eid_2-s2.0-0023682695
- PMID: 2456165
- WOS: WOS:A1988P634600019
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Cardiac response to pressure overload in the rat: The selective alteration of in vitro directed RNA translation products
Title | Cardiac response to pressure overload in the rat: The selective alteration of in vitro directed RNA translation products |
---|---|
Authors | |
Issue Date | 1988 |
Citation | Circulation Research, 1988, v. 63 n. 2, p. 448-456 How to Cite? |
Abstract | As cardiac hypertrophy develops, total cardiac RNA and protein synthesis increase significantly. We have identified specific messenger RNAs that change in predominance with the induction of pressure-overload-stimulated cardiac hypertrophy. Total cardiac RNA was isolated from rats either undergoing cardiac hypertrophy secondary to subdiaphragmatic aortic constriction or subjected to sham surgery. The products translated in vitro were separated by two-dimensional gel electrophoresis and quantitated. The translation of four proteins decreased while the translation of four others increased in preparations from hypertrophied hearts compared with those from sham-treated rats. Two isoforms of creatine kinase M were translated in vitro. Only one of these isoforms decreased with cardiac hypertrophy, suggesting that the transcriptional or translation control for creatine kinase is much more complex than previously believed. Finally, since only eight of over 700 different translation products change in relative predominance with cardiac hypertrophy, we conlude that the accumulation of existing RNA and protein products is the primary adaptive process responsible for cardiac hypertrophy. |
Persistent Identifier | http://hdl.handle.net/10722/195216 |
ISSN | 2023 Impact Factor: 16.5 2023 SCImago Journal Rankings: 4.903 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Boheler, KR | - |
dc.contributor.author | Dillmann, WH | - |
dc.date.accessioned | 2014-02-25T01:40:19Z | - |
dc.date.available | 2014-02-25T01:40:19Z | - |
dc.date.issued | 1988 | - |
dc.identifier.citation | Circulation Research, 1988, v. 63 n. 2, p. 448-456 | - |
dc.identifier.issn | 0009-7330 | - |
dc.identifier.uri | http://hdl.handle.net/10722/195216 | - |
dc.description.abstract | As cardiac hypertrophy develops, total cardiac RNA and protein synthesis increase significantly. We have identified specific messenger RNAs that change in predominance with the induction of pressure-overload-stimulated cardiac hypertrophy. Total cardiac RNA was isolated from rats either undergoing cardiac hypertrophy secondary to subdiaphragmatic aortic constriction or subjected to sham surgery. The products translated in vitro were separated by two-dimensional gel electrophoresis and quantitated. The translation of four proteins decreased while the translation of four others increased in preparations from hypertrophied hearts compared with those from sham-treated rats. Two isoforms of creatine kinase M were translated in vitro. Only one of these isoforms decreased with cardiac hypertrophy, suggesting that the transcriptional or translation control for creatine kinase is much more complex than previously believed. Finally, since only eight of over 700 different translation products change in relative predominance with cardiac hypertrophy, we conlude that the accumulation of existing RNA and protein products is the primary adaptive process responsible for cardiac hypertrophy. | - |
dc.language | eng | - |
dc.relation.ispartof | Circulation Research | - |
dc.title | Cardiac response to pressure overload in the rat: The selective alteration of in vitro directed RNA translation products | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1161/01.RES.63.2.448 | - |
dc.identifier.pmid | 2456165 | - |
dc.identifier.scopus | eid_2-s2.0-0023682695 | - |
dc.identifier.volume | 63 | - |
dc.identifier.issue | 2 | - |
dc.identifier.spage | 448 | - |
dc.identifier.epage | 456 | - |
dc.identifier.isi | WOS:A1988P634600019 | - |
dc.identifier.issnl | 0009-7330 | - |