Endocardium of the Left Ventricle in Volume‐loaded Canine Heart

Masuda, Hirotake; Kawamura, Koichi; Tohda, Kohei; Shozawa, Takeshi; Sato, Masato; Honma, Makiko

doi:10.1111/j.1440-1827.1989.tb01488.x

Cited by 2 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The role of the EE in these diseases has only recently been addressed. Typical morphological EE cellular lesions have now been described in conditions of ventricular volume (361) or pressure (81, 541) overloading, in experimental diabetes FIG. 11. Role of endothelial dysfunction in the progression of chronic cardiac failure.…”

Section: Cardiac Endothelial Dysfunction In Cardiac Failurementioning

confidence: 94%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

606

544

View full text Add to dashboard Cite

Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.

show abstract

Section: Cardiac Endothelial Dysfunction In Cardiac Failurementioning

confidence: 94%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

606

544

View full text Add to dashboard Cite

show abstract

“…Since bFGF has been shown to play a role in autocrine growth regulation (44) and migration (29) of the endothelial cell, this high shear-induced increase may be relevant to the observed long-term increase in endothelial density that is oh served following surgically induced increases in blood flow in the canine carotid artery arteriovenous shunt model (4 4 h. In contrast our study showed that both physiological moderate ( 15 dyn/cm2) and elevated ( 36 dyn/cm2) shear stress induced a marked four-to fivefold decrease in PDGF B chain mRNA by 6-9 h. The BAE cells, unlike HUVE cells, express the B but not the A chain ofPDGF (39); the difference in the results may be due to the difference in cell origin. Furthermore, changes in mRNA levels were not reported for durations of shear > 4 h, the time after which the downregulation reported in the present work is most significant.…”

Section: =2060mentioning

confidence: 99%

“…We also hypothesized that shear stress may affect the expression of bFGF in light of the findings ofincreased endothelial density in response to step increases to high flow and resulting high shear stress (4). We have evaluated the in vitro effect of fluid shear stress of physiological moderate (15 dyn/cm2) and elevated (36 dyn/cm2) magnitude on the morphological properties and extent of cell shape change in confluent BAE monolayers and on mRNA levels of PDGF-B and bFGF using a previously described cone-plate apparatus (20).…”

Section: Introductionmentioning

confidence: 99%

Fluid shear stress differentially modulates expression of genes encoding basic fibroblast growth factor and platelet-derived growth factor B chain in vascular endothelium.

Malek

Gibbons²,

Dzau³

et al. 1993

J. Clin. Invest.

274

142

View full text Add to dashboard Cite

Fluid shear stress has been shown to be an important regulator of vascular structure and function through its effect on the endothelial cell. We have explored the effect of shear stress on the expression of the heparin-binding growth factors platelet-derived growth factor B chain (PDGF-B) and basic fibroblast growth factor (bFGF) in bovine aortic endothelial cells using a purpose-built cone-plate viscometer. Using morphometric analysis, we have mimicked the endothelial cell shape changes encountered in vivo in response to shear stress and correlated these with changes in gene expression. Steady laminar shear stress of 15 and 36 dyn/cm2 both resulted in endothelial cell shape change, but the higher shear stress induced greater and more uniform alignment in the direction of flow and nuclear protrusion after 24 h. Steady laminar shear stress of both 15 and 36 dyn/cm2 induced a significant 3.9-and 4.2-fold decrease, respectively, in PDGF-B mRNA at 9 h. In contrast, steady laminar shear of 15 dyn/cm2 induced a mild and transient 1.5-fold increase in bFGF mRNA while shear of 36 dyn/ cm2 induced a significant 4.8-fold increase at 6 h of shear which remained at 2.9-fold at 9 h. Pulsatile and turbulent shear stress showed the same effect as steady laminar shear stress (all at 15 dyn/cm2 time-average magnitude) on PDGF-B and bFGF mRNA content. Cyclic stretch (20% strain, 20/min) of cells grown on silicone substrate did not significantly affect either PDGF-B or bFGF mRNA levels. These results suggest that expression of each peptide growth factor gene is differentially regulated by fluid shear stress in the vascular endothelial cell. These results may have implications on vascular structure and function in response to hemodynamic forces and present a model for the study of transduction of mechanical stimuli into altered gene expression. (J. Clin.

show abstract

Endocardium of the Left Ventricle in Volume‐loaded Canine Heart

Cited by 2 publications

References 17 publications

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Fluid shear stress differentially modulates expression of genes encoding basic fibroblast growth factor and platelet-derived growth factor B chain in vascular endothelium.

Contact Info

Product

Resources

About