Abstract:
:This study addressed the question whether the molecular mass of proteins influences their release from isolated rat neonatal cardiomyocytes subjected to simulated ischemia (SI) or metabolic inhibition (MI). During these interventions cellular ATP content and the relative releases of several proteins, ranging in molecular mass from 15 to 140 kDa, were determined. After 180 min of normoxia, cellular ATP content was about 90% of the initial value, and cellular protein loss was about 1%. During either SI (180 min) or MI (120 min) the cellular ATP content decreased to less than 5% of the initial value. After 180 min of SI the release of soluble cytoplasmic proteins from the cells had increased to about 35%, and after 120 min of MI to about 90%. There were no major differences in the release pattern of four cytoplasmic proteins, during both SI and MI. A soluble mitochondrial and a partly mitochondrial protein, however, showed delayed release patterns. These data indicate that the release of proteins from damaged isolated neonatal rat cardiomyocytes is not related to the molecular mass of the proteins. It is concluded that protein release from damaged cardiomyocytes is not a sieving process in which small proteins are preferentially lost. In contrast, our data suggest that sarcolemmal disruption is a relatively fast process resulting in the simultaneous release of all soluble cytoplasmic proteins, irrespective of their molecular mass.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Van Nieuwenhoven FA,Musters RJ,Post JA,Verkleij AJ,Van der Vusse GJ,Glatz JFdoi
10.1006/jmcc.1996.0133subject
Has Abstractpub_date
1996-07-01 00:00:00pages
1429-34issue
7eissn
0022-2828issn
1095-8584pii
S0022-2828(96)90133-9journal_volume
28pub_type
杂志文章abstract::Cell therapy has the potential to drastically improve clinical outcomes for the 1.45 million patients suffering from a myocardial infarction (MI) each year in the U.S. However, the limitations associated with this treatment - including poor engraftment, significant cell death and poor differentiation potential - have ...
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pub_type: 杂志文章,评审
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更新日期:2012-01-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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doi:10.1006/jmcc.1999.0985
更新日期:1999-08-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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更新日期:1986-09-01 00:00:00
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pub_type: 杂志文章,评审
doi:10.1006/jmcc.2001.1376
更新日期:2001-05-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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更新日期:2010-05-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/s0022-2828(88)80025-7
更新日期:1988-02-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2004.01.009
更新日期:2004-05-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2010.10.019
更新日期:2011-01-01 00:00:00
abstract::Experimental evidence has emerged that myocardial ischemic preconditioning can prime the mitochondria into a "stress-resistant state", so that cell death is reduced following prolonged severe ischemia and reperfusion. Using a swine model of chronically ischemic myocardium, we tested the hypothesis that mitochondria wi...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2006.07.008
更新日期:2006-12-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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更新日期:2011-04-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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doi:10.1006/jmcc.1993.1077
更新日期:1993-06-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2001-01-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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更新日期:2013-07-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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更新日期:2020-06-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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abstract::In recently published studies, we show that angiotensin II (AII) generated from an engineered rat angiotensinogen cDNA, and maintained intracellularly, is growth stimulatory for a rat hepatoma cell line. In the present study, we report that co-expression of AII fused to cyan fluorescent protein (ECFP/AII) and angioten...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2003.09.021
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abstract::Reoxygenation of isolated rat cardiac myocytes following a period of hypoxia and substrate deprivation resulted in a 1.5-2-fold increase in the total Ca2+ content which could be inhibited by 1 microM antimycin A or ruthenium red (50% inhibition at 2.5 microM). This increase in Ca2+ content was not accompanied by any r...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/0022-2828(89)90795-5
更新日期:1989-10-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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abstract::Adequate wound healing and scar formation is an essential response to myocardial infarction (MI), and fibroblasts are primary cellular components regulating the process. How fibroblast functions are altered post-MI and to what extent these abnormalities persist in vitro is not well understood. Accordingly, we isolated...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2005.07.008
更新日期:2005-10-01 00:00:00
abstract::We previously established a new measuring method of the myocardial O2 consumption of mechanically unloaded rat left-ventricular slices. O 2 consumption of unstimulated myocardium corresponds to basal metabolism. We have found O2 consumption of stimulated myocardium to include basal metabolism and O 2 consumption for C...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1997.0630
更新日期:1998-03-01 00:00:00
abstract::Increasing bodies of evidence indicate that reactive oxygen species (ROS) produced by mitochondria and other sources play an essential role in mediating ventricular remodeling after myocardial infarction and the development of heart failure. Antioxidants scavenge ROS, thereby maintaining the reduced environment of cel...
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pub_type: 杂志文章,评审
doi:10.1016/j.yjmcc.2006.08.006
更新日期:2006-11-01 00:00:00