Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Severson, David L.; Carroll, Rogayah; Kryski, Albert; Ramı́rez, Ignasi

doi:10.1042/bj2480289

Cited by 13 publications

(13 citation statements)

References 30 publications

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“…of 4 x 105 cells/ml, and were incubated at 37°C under 02/CO2 (19:1). The release of LPL into the incubation medium was measured as described previously [14][15][16]. Heparin was added to the myocyte incubation medium to give a final concentration of 5 units/ml, and at various times 1 ml samples were removed and centrifuged for 10 s at 15000 g in an Eppendorf centrifuge.…”

Section: Methodsmentioning

confidence: 99%

“…5 %, v/v) was added to the cultured myocytes in 1 ml ofJoklik medium. After centrifugation, the deproteinized supernatant was neutralized and cyclic AMP was measured by radioassay [16,17].…”

Section: Methodsmentioning

confidence: 99%

“…The heparin-induced release of LPL into the incubation medium of cardiac myocytes [13-151 is characterized by two phases: a rapid release (5-10 min) from sites that are presumably at or near the myocardial cell surface [14,15], followed by a slower rate of release (10-120 min) that is dependent on protein synthesis and microtubular function [13][14][15]. A short-term preincubation (30 min) of cardiac myocytes with isoprenaline or forskolin did not change cellular or heparin-releasable LPL activities measured after a 5-10 min incubation with heparin [16]. The objective of the present investigation was to determine if the slow protein-synthesisdependent phase of LPL secretion in response to heparin could be influenced by incubation of cardiac myocytes with forskolin or a cyclic AMP analogue, 8-(4-chlorophenylthio)adenosine 3',5'cyclic monophosphate (CPT-cAMP).…”

Section: Introductionmentioning

confidence: 92%

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Treatment of cardiac myocytes with 8-(4-chlorophenylthio)-adenosine 3′,5′-cyclic monophosphate, forskolin or cholera toxin does not stimulate cellular or heparin-releasable lipoprotein lipase activities

Carroll

Juhasz

Severson

1990

Biochemical Journal

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Incubation of isolated cardiac myocytes with 500 microM-8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate (CPT-cAMP) or 100 microM-forskolin for 2 1/2 h did not increase the heparin-induced release of lipoprotein lipase (LPL) into the medium. When LPL activity in cardiac myocytes was depleted by treatment of rats with cycloheximide (2 mg/kg; 2.5 h) and inclusion of the protein-synthesis inhibitor in the isolation solutions, incubation with CPT-cAMP or forskolin did not influence the rate of repletion of LPL activity in cells or the recovery of heparin-releasable LPL activity. Although the administration of cholera toxin (0.5 mg/kg; 16-17 h) to rats increased LPL activity in a low-speed supernatant fraction from heparin-perfused hearts, LPL activity was not increased in cardiac myocytes from cholera-toxin-treated rat hearts, and the heparin-induced release of LPL was unchanged. Incubation of cultured ventricular myocytes with 1 microgram of cholera toxin/ml or 500 microM-CPT-cAMP for 24 h did not increase cellular LPL activity or LPL released into the culture medium after a 40 min incubation with heparin. Therefore interventions that stimulate adenylate cyclase activity (forskolin, cholera toxin) or incubation with CPT-cAMP do not increase cellular LPL activity or promote the translocation of LPL to a heparin-releasable fraction in cardiac myocytes.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

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Treatment of cardiac myocytes with 8-(4-chlorophenylthio)-adenosine 3′,5′-cyclic monophosphate, forskolin or cholera toxin does not stimulate cellular or heparin-releasable lipoprotein lipase activities

Carroll

Juhasz

Severson

1990

Biochemical Journal

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“…Previous studies have shown that incubation of cardiomyocytes with Iso for 30 min had no effect on either basal or HR-LPL activity (60). In the present study, incubation with this ␤-agonist was Values are means Ϯ SE for 6 animals in each group.…”

Section: Coronary Luminal Lpl Activity Increases After a Single Dose mentioning

confidence: 53%

“…Thus, even though the majority of enzyme is located in myocytes, vascular endothelial-bound LPL likely determines the rate of plasma lipoprotein-TG clearance (41). Previously, incubation of cardiomyocytes with Iso for 30 min did not change either HR-LPL or cellular LPL activity (60). We have confirmed these findings even after incubation with Iso was prolonged for 1 h. Because cardiomyocytes are quiescent, we extended these experiments to an isolated retrograde perfused heart and demonstrated a similar absence of effect of this ␤-agonist on LPL.…”

Section: Discussionmentioning

confidence: 97%

β-Agonist stimulation produces changes in cardiac AMPK and coronary lumen LPL only during increased workload

Ding

Kewalramani

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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(LPL) in cardiac and vascular pathology, the objective of the present study was to investigate whether the ␤-agonist isoproterenol (Iso) influences cardiac LPL. Incubation of quiescent cardiomyocytes with Iso for 60 min had no effect on basal, intracellular, or heparin-releasable (HR)-LPL activity. Similarly, Iso did not change HR-LPL in Langendorff isolated hearts that do not beat against an afterload. In the intact animal, LPL activity at the vascular lumen increased significantly in the Isotreated group, together with a substantial increase in rate-pressure product. This LPL increase was likely via mechanisms regulated by activation of AMP-activated protein kinase (AMPK) and inactivation of acetyl-CoA carboxylase (ACC280). In glucose-perfused hearts, simply switching from Langendorff to the isolated working heart (that beats against an afterload) induced increases in AMPK and ACC280 phosphorylation and enhanced HR-LPL activity. Provision of insulin and albumin-bound palmitic acid to the working heart was able to reverse these effects. In these hearts, introduction of Iso to the buffer perfusate duplicated the effects seen when this ␤-agonist was given in vivo. Our data suggest that Iso can influence HR-LPL only during conditions of increased workload, mechanical performance and excessive energy expenditure, and likely in an AMPK-dependent manner.isoproterenol; acetyl-coenzyme A carboxylase; cardiomyocyte; Langendorff heart; working heart; adenosine 3Ј,5Ј-monophosphate-activated protein kinase; lipoprotein lipase CARDIAC CONTRACTILITY REQUIRES an uninterrupted supply of ATP. Under normal physiological conditions, the heart utilizes two major substrates, glucose and fatty acids (FA; see Ref. 51). Compared with glucose, FA is the preferred substrate and accounts for ϳ70% of ATP production. However, the heart has the ability to choose its substrates depending on their availability and the prevailing physiological (e.g., exercise) or pathophysiological (e.g., ischemia) conditions. AMP-activated protein kinase (AMPK) is likely a key player in modulating this substrate selection. Thus, during exercise (when ATP expenditure is augmented) or ischemia (when manufacture of ATP is hindered), changes in intracellular AMP/ATP levels promote threonine (Thr 172 ) phosphorylation and activation of AMPK (22,25). Upon stimulation, AMPK switches off energy-consuming processes like triglyceride (TG) and protein synthesis, whereas ATP-generating mechanisms are turned on (21, 26). In heart and skeletal muscle, phosphorylated AMPK stimulates glucose uptake (23, 55) and subsequent glycolysis through the activation of 6-phosphofructo-2-kinase (38). More importantly, through its control of acetyl-CoA carboxylase (ACC), AMPK facilitates FA oxidation (31, 32). AMPK has also been implicated in FA delivery to cardiomyocytes through its regulation of the FA transporter, CD36 (36). Finally, results from our laboratory have demonstrated a strong correlation between activation of cardiac AMPK and increases in coronary lumen lipoprotein lipas...

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Hormones and triacylglycerol metabolism under normoxic and ischemic conditions

Schoonderwoerd

Kraaij

Hülsmann

et al. 1989

Lipid Metabolism in Normoxic and Ischemic Heart

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Short-term incubation of cardiac myocytes with isoprenaline has no effect on heparin-releasable or cellular lipoprotein lipase activity

Cited by 13 publications

References 30 publications

Treatment of cardiac myocytes with 8-(4-chlorophenylthio)-adenosine 3′,5′-cyclic monophosphate, forskolin or cholera toxin does not stimulate cellular or heparin-releasable lipoprotein lipase activities

Treatment of cardiac myocytes with 8-(4-chlorophenylthio)-adenosine 3′,5′-cyclic monophosphate, forskolin or cholera toxin does not stimulate cellular or heparin-releasable lipoprotein lipase activities

β-Agonist stimulation produces changes in cardiac AMPK and coronary lumen LPL only during increased workload

Hormones and triacylglycerol metabolism under normoxic and ischemic conditions

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