Prostacyclin synthesis by proliferative aortic smooth muscle cells A kinetic in vivo and in vitro study

Larrue, J; Daret, Danièle; Demond-Henri, J.; Allières, Cécile; Bricaud, H

doi:10.1016/0021-9150(84)90008-x

Cited by 26 publications

(6 citation statements)

References 22 publications

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“…PGF^ synthesis was not determined. Larrue et al 104 also compared the prostaglandin synthetic activity of rabbit aortic smooth muscle cells in intact artery and in culture. PGEa, PGI 2 , and PGF^ were all synthesized in response to addition of arachidonic acid.…”

Section: Eicosanoidsmentioning

confidence: 99%

“…107 Cultured rabbit aortic smooth muscle cells have been shown to generate lipoxygenase products from exogenous arachidonic acid. 104 Human umbilical arterial smooth muscle cells generate PGE^, PGI 2 , PGF^, 12-hydroxyheptadecatrienoic acid, and 11-hydroxy-eicosatetraenoic acid from exogenous arachidonate in vitro. 108 PGE 2 is the major metabolite.…”

Section: Eicosanoidsmentioning

confidence: 99%

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Pharmacology of smooth muscle cell replication.

1992

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The suggestion that smooth muscle cell proliferation contributes to hypertension, atherosclerosis, and restenosis after angioplasty has led to a growing interest in the use of drugs to inhibit this process. This review summarizes pharmacological studies of smooth muscle cell proliferation in vitro and in vivo and identifies specific mediators of proliferation that are implicated by drugs binding with high affinity to enzymes or receptors. (Hypertension 1992^0:713-736) KEY WORDS • atherosclerosis • growth substances • hypertension, essential • muscle, smooth, vascular T his review emphasizes agents that influence smooth muscle proliferation. Four overlapping categories of agents that could be discussed are growth factors, drugs with known pharmacological effects, endocrine hormones with growth regulatory properties, and intracellular mediators of replication. This review will concentrate on the last three categories. A great deal has already been written in other reviews about the growth factors, but the much longer list of possible targets discussed here has not been reviewed systematically. Moreover, a great deal is known about the pharmacology of some of the molecules in our review, so their therapeutic value in the treatment of conditions arising from smooth muscle replication is likely to be realized more quickly in a clinical sense than treatments based on the still very poorly understood pharmacology of growth factors. Pathology of Smooth Muscle ProliferationSmooth muscle proliferation has been implicated as playing a central role in atherosclerosis and hypertension.1 The evidence that smooth muscle cell proliferation occurs in these diseases is clear. As we will briefly review, however, evidence for a causal connection is not well established. Smooth Muscle Replication in HypertensionThe argument for a role of smooth muscle cell replication in hypertension is an outgrowth of the structural hypothesis of hypertension proposed by Folkow.2 Folkow explained that the ability of a resistance artery to restrict blood flow depends on the thickness of the vessel wall as well as on the size of the vessel lumen, the responsiveness of the wall to vasoactive stimuli, and the level of stimulation by vasoconstrictors. Folkow's idea is based on the simple physical fact that a thicker vessel wall will act as an amplifier, so that an equal vasoconstrictor stimulus will produce greater narrowing of the lumen in a hypotensive vessel than in a normotensive vessel. Studies of essential and secondary hypertension have confirmed that hypertensive vessel walls are thickened.3 Indeed, there is evidence that such structural changes precede any elevation in blood pressure,*-5 and, at least for the spontaneously hypertensive rat, wall thickening may depend on the increased sympathetic innervation that develops in the spontaneously hypertensive rat vessel wall within the first month of life. 5 -6 A correlation exists between the development of sympathetic innervation and the development of arterial medial hypertrophy in normotensive...

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Section: Eicosanoidsmentioning

confidence: 99%

Section: Eicosanoidsmentioning

confidence: 99%

Pharmacology of smooth muscle cell replication.

1992

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“…1C), and the changes persist up to 3 weeks after endothelial injury (Knieriem et al, 1973;Fishman et al, 1975;Schwartz et al, 1975;Spaet et al, 1975;Clowes and Karnovsky, 1977;Guyton and Karnovsky, 1979;Haudenschild and Schwartz, 1979;Taura et al, 1979;Campbell et al, 1983;Clowes et al, 1983;Larrue et al, 1984). Upon reestablishment of the overlying endothelial layer, the smooth muscle cells of the neointima return to the contractile state, regaining an apparently normal complement of myofilaments with a concomitant decrease in the amount of synthetic organelles (Clowes et al, 1983;Larrue et al, 1984). This sequence is also seen in biochemical and immunocytochemical studies of the expression of contractile and cytoskeletal proteins.…”

Section: Phenotypic Expression In Artery Regenerationmentioning

confidence: 99%

Replication of smooth muscle cells in vascular disease.

Schwartz¹,

Campbell²,

Campbell³

1986

Circulation Research

681

378

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SUMMARY. Smooth muscle proliferation has been recognized as central to the pathology of both major forms of vascular disease: atherosclerosis and hypertension. Recent advances in our knowledge of mechanisms of control of proliferation suggest that events occurring in adult animals may recapitulate portions of the developmental biology of the smooth muscle cell. This review attempts to consider the current state of knowledge of the mechanisms controlling smooth muscle proliferation in these two diseases, to put that knowledge into the context of what is known about smooth muscle biology, and to offer two hypotheses on the possible roles of smooth muscle developmental biology in manifestations of atherosclerosis and hypertension in adult humans. (Circ Res 58: 427-444, 1986)

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“…Prostaglandin production by endothelial and vascular smooth muscle cells has been extensively studied in separate cultures of these cells (Samuelsson et al, 1978;Smith, 1986;Weksler, 1984;Larrue et al, 1984;Dejana et al, 1983;DeWitt et al, 1983). Prostacyclin is the principal prostaglandin produced by endothelial cells from a number of different sources (Samuelsson et al, 1978;Smith, 1986;Weksler, 1984).…”

mentioning

confidence: 99%

“…Prostaglandin production in different populations of cultured smooth muscle cells appears to be more variable. Some authors have reported prostacyclin to be the primary smooth muscle cell prostaglandin (Larrue et al, 1984;Dejana et al, 1983), while others have reported principally prostaglandin E2 (PGE2) (Ager et al, 1982) or equal amounts of prostaglandin E2 (PGE2) and prostaglandin Faa (PGF2J (Ody et al, 1982). However, until recently it has not been possible to examine prostaglandin production by both cell types when grown together, as they exist in the vessel wall.…”

mentioning

confidence: 99%

Lipid transfer between endothelial and smooth muscle cells in coculture

Stoll

Spector

1987

Journal Cellular Physiology

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A coculture system was employed to study the interactions between endothelium and vascular smooth muscle cells in arachidonic acid metabolism. Bovine aortic endothelial cells grown on micropore filters impregnated with gelatin and coated with fibronectin are mounted on polystyrene chambers and suspended over confluent smooth muscle cultures. The endothelial basal laminae are oriented toward the underlying smooth muscle, and the two layers are separated by only 1 mm. Each cell layer was assayed individually: apical and basolateral fluid also was collected separately for assay. Fatty acids, including arachidonic acid, are readily transferred between the endothelial and smooth muscle cells in this system. Distribution of the incorporated fatty acids among the lipids of each cell is the same as when the fatty acid is added directly to the culture medium. Arachidonic acid released from endothelial cells is available as a substrate for prostaglandin production by smooth muscle. In addition, fatty acids released from the smooth muscle cells can pass through the endothelium and accumulate in the fluid bathing the endothelial apical surface. These fatty acid interchanges may be involved in cell-cell signaling within the vascular wall, the clearance of lipids from the vascular wall, or the redistribution of arachidonic acid and other polyunsaturated fatty acids between adjacent cell types. Furthermore, the findings suggest that prostaglandin production by smooth muscle cells can occur in response to stimuli that cause arachidonic acid release from endothelial cells.

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Prostacyclin synthesis by proliferative aortic smooth muscle cells A kinetic in vivo and in vitro study

Cited by 26 publications

References 22 publications

Pharmacology of smooth muscle cell replication.

Pharmacology of smooth muscle cell replication.

Replication of smooth muscle cells in vascular disease.

Lipid transfer between endothelial and smooth muscle cells in coculture

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