Production of arachidonic acid metabolites in adult rat cardiac myocytes, endothelial cells, and fibroblast-like cells

Linssen, M. C. J. G.; Engels, W.; Lemmens, P. J. M. R.; Heijnen, V. V. T.; Bilsen, Marc van; Reneman, Robert S.; Vusse, Ger J.

doi:10.1152/ajpheart.1993.264.3.h973

Cited by 18 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Endothelial cells and fibroblasts exist in close proximity to cardiac myocytes, and the PGs they produce may affect neighboring myocardial cells. Culture medium concentrations of PGF 2␣ from unstimulated primary cultures of three types of adult rat heart cells revealed the following order of production: endothelial cells Ͼ fibroblast-like cells Ͼ myocytes (45). Similar results were reported for neonatal rat fibroblast-like cells and myocytes (46).…”

Section: Discussionsupporting

confidence: 82%

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Adams

Migita²,

Yu³

et al. 1996

Journal of Biological Chemistry

View full text Add to dashboard Cite

During embryonic development the myocardium enlarges by the proliferation of cardiac myocytes. Shortly after birth, cardiac myocytes lose their capacity for mitogenesis, and further growth of the myocardium to meet the increasing hemodynamic demand of an elevated blood pressure and blood volume occurs by enlargement of existing muscle cells (hypertrophy). Similarly, the restoration of myocardial contractile performance lost to ischemia or viral infection is dependent on the recovery of injured myocytes and on the compensatory enlargement of agonist myocytes. Thus, an understanding of the controlling factors of myocardial protein synthesis and growth has implications for cardiac ontogeny, adaptation to chronic physiologic and pathophysiologic stimuli, and recovery from injury.Cardiac hypertrophy is produced by a variety of stimuli in culture and in vivo (1), including, but not limited to, mechanical stretch (2, 3), neurotransmitters (4, 5), and hormones (6, 7). As the biochemistry of myocardial growth is experimentally revealed, some common intracellular signaling pathways appear among primary stimuli. For example, stretch-induced cardiomyocyte hypertrophy is mediated, in part, by the local production of angiotensin II (8), and several hypertrophic stimuli, angiotensin II, norepinephrine, and endothelin-1, act through G q protein-coupled receptors (9 -11) and activate mitogen-activated protein kinases (12, 13). Direct evidence of G q involvement in cardiac growth was provided by microinjection of G q neutralizing antibodies to block the hypertrophic response of neonatal rat ventricular myocytes to the ␣ 1 -adrenergic agonist phenylephrine (9). Thus cardiac hypertrophy appears to be mediated, at least for several stimuli, by agonists of G q proteincoupled receptors.In addition to promoting myocardial growth, angiotensin II, norepinephrine, and endothelin-1 are vasoactive substances. Interestingly, Katz (14) speculated that angiotensin II evolved from a primitive growth factor and assumed additional regulatory roles in the cardiovascular system, such as stimulation of aldosterone production and smooth muscle contraction. It is conceivable that other vasoactive substances went through a similar evolutionary process, especially in consideration of the finding that Ca 2ϩ signaling is important for angiotensin II activation of mitogen-activated protein kinase in cardiac myocytes (13).Prostaglandin F 2␣ (PGF 2␣ ) 1 is a vasoactive substance that stimulates protein synthesis in skeletal and smooth muscle cells in culture (15,16). Moreover, PGF 2␣ regulates, in part, stretch-induced skeletal myoblast growth (16), and the effects of exogenous PGF 2␣ on vascular smooth muscle hypertrophy are most likely mediated by a PGF-specific receptor (15). As to the heart, PGF 2␣ was increased in the left ventricles of rabbits by acute pressure overload (17), and PG synthase inhibitors blocked cardiac growth induced by hypertension (18) and clenbuterol (19). These observations and others suggested that PGF 2␣ may play a role in the con...

show abstract

Section: Discussionsupporting

confidence: 82%

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Adams

Migita²,

Yu³

et al. 1996

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown increased release of thromboxane A 2 in myocardial ischemia and production of arachidonic metabolites in the ischemic myocardium and in cardiac myocytes under physiological and stimulated conditions. 7,8,10 In addition, Liu et al 11 have recently shown the presence of both COX-1 and COX-2 in the normal and lipopolysaccharide-stimulated rat heart. The latter study supports our findings of induced COX-2 expression in the myocytes and inflammatory cells of patients with heart failure secondary to sepsis.…”

Section: Discussionmentioning

confidence: 97%

“…2 In addition to cytokines, hypoxia, an important feature of ischemic myocardium, induces COX-2 (via NF-B) in cultured endothelial cells independently of other stimuli. 5 Although there have been several studies that demonstrated induction of COX-2 and its association with NF-B activation in various cells, 2,3 and despite the numerous studies describing the production of prostanoids in myocytes, 6,7 whether or not COX-2 is expressed in the human myocardium remains to be elucidated. Interest in COX-2 expression in the failing heart is heightened by the diverse inotropic and morphological effects of prostaglandins on the heart.…”

mentioning

confidence: 99%

Induction of Cyclooxygenase-2 and Activation of Nuclear Factor-κB in Myocardium of Patients With Congestive Heart Failure

et al. 1998

View full text Add to dashboard Cite

Background —Chronic heart failure is associated with induction of secondary inflammatory mediators, including prostanoids. The latter exert diverse functional and morphological effects on cardiac myocytes. Induction of cyclooxygenase (COX), the enzyme responsible for generating prostanoids, requires activation of nuclear factor-κB (NF-κB). The aim of the present study was to determine the expression of COX-2 and activation of NF-κB in the failing human heart. Methods and Results —Myocardial tissue from 27 patients with end-stage heart failure (various etiologies: ischemic heart disease, n=16; idiopathic dilated cardiomyopathy, n=10; and valvular heart disease, n=1), 2 septic patients, and 8 normal control subjects was immunostained with antisera to COX-2 and NF-κB. Western blotting was performed and showed high anti–COX-2 antibody specificity and the presence of COX-2 protein in the sample tissues. In situ hybridization and immunohistochemistry showed little or no expression of COX-2 and NF-κB in the control hearts. In contrast, there was abundant expression of COX-2 mRNA and protein in myocytes and inflammatory cells in areas of fibrotic scar compared with regions of normal morphology in all cases of heart failure, except the cases with sepsis, which showed an abundance of COX-2 throughout the myocardium. Sites of NF-κB activation were associated with those of COX-2 expression. Conclusions —We demonstrate induction of COX-2 and activation of NF-κB in the myocardium of failing human hearts. Induction of both molecules appears to be associated with the presence of inflammation and scar formation.

show abstract

“…However, TxA 2 generation has been noted in vascular smooth muscle and endothelial cells of the rat and formation of cys-LTs in endothelium-adherent leukocytes, myocytes, and resident mast cells in the rat heart (32)(33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Free arachidonic versus eicosapentaenoic acid differentially influences the potency of bacterial exotoxins to provoke myocardial depression in isolated rat hearts

Grandel

Benkelmann²,

Buerke³

et al. 2006

Critical Care Medicine

View full text Add to dashboard Cite

show abstract

Production of arachidonic acid metabolites in adult rat cardiac myocytes, endothelial cells, and fibroblast-like cells

Cited by 18 publications

References 0 publications

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Induction of Cyclooxygenase-2 and Activation of Nuclear Factor-κB in Myocardium of Patients With Congestive Heart Failure

Free arachidonic versus eicosapentaenoic acid differentially influences the potency of bacterial exotoxins to provoke myocardial depression in isolated rat hearts

Contact Info

Product

Resources

About