Culture of rat mesenteric arteriolar smooth muscle cells: effects of platelet-derived growth factor, angiotensin, and nitric oxide on growth

Dubey, Raghvendra K.; Overbeck, Henry W.

doi:10.1007/bf00305381

Cited by 29 publications

(12 citation statements)

References 21 publications

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“…It is well-documented that NO, generated by eNOS, inhibits proliferation of a number of cell types including VSMC and lymphocytes thus prevents the initiation and/or progression of atherosclerotic disease [25,26]. It is also well-known that ROS, produced by NAD(P)H oxidase, determine bioavailability of NO in the cardiovascular system and are implicated in the pathogenesis of atherosclerosis through their ability to enhance VSMC proliferation and migration [13,14].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide synthase and NAD(P)H oxidase modulate coronary endothelial cell growth

Bayraktutan

2004

Journal of Molecular and Cellular Cardiology

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Reactive oxygen species (ROS) including nitric oxide (NO) and superoxide anion (O 2 -) are associated with cell migration, proliferation and many growth-related diseases. The objective of this study was to determine whether there was a reciprocal relationship between rat coronary microvascular endothelial cell (CMEC) growth and activity/expressions (mRNA and protein) of endothelial NO synthase (eNOS) and

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Section: Discussionmentioning

confidence: 99%

Nitric oxide synthase and NAD(P)H oxidase modulate coronary endothelial cell growth

Bayraktutan

2004

Journal of Molecular and Cellular Cardiology

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“…The endothelium is an important vascular structure because it produces mediators regulating vascular tone, vascular growth, platelet function and coagulation [10, 42, 43, 44]. A previous report showed a close relationship between the magnitude of endothelium-dependent vasodilation in coronary artery and that of brachial artery [21].…”

Section: Discussionmentioning

confidence: 99%

The Relationship of Left Ventricular Mass to Endothelium-Dependent Vasodilation of the Brachial Artery in Patients with Hypertension

Motoyama¹,

Kawano²,

Hirai³

et al. 2001

Cardiology

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Although echocardiographically determined left ventricular mass and geometry predict cardiovascular morbid events in patients with hypertension, the mechanisms underlying this relation are unclear. There is considerable evidence that endothelium-dependent vasodilation is impaired in patients with hypertension. Thus, endothelial dysfunction may contribute to the mechanism that causes cardiovascular morbid events. This study was designed to examine the relationship between left ventricular geometry and endothelial function in patients with hypertension. The percentage increase in brachial arterial diameter during reactive hyperemia was examined by a high-resolution ultrasound technique in 49 patients with hypertension and 64 normotensive subjects. Patients with hypertension had an impairment of the percentage increase in brachial arterial diameter during reactive hyperemia and an increase in thiobarbituric acid-reactive substances (TBARS) compared to normotensive subjects (percentage increase in diameter 5.6 ± 3.0 vs. 8.0 ± 2.5%, p < 0.001; TBARS levels 6.1 ± 1.3 vs. 5.3 ± 1.0 nmol/ml, p < 0.001). In patients with hypertension, there was a significant correlation between the left ventricular mass index and the percentage increase in brachial arterial diameter during reactive hyperemia (r = –0.583, p < 0.001), and the percentage increase in brachial arterial diameter during reactive hyperemia varied with the pattern of left ventricular geometry (normal ventricular geometry: 7.7 ± 2.6%; concentric remodeling: 5.2 ± 2.3%; eccentric hypertrophy: 4.2 ± 1.8%; concentric hypertrophy: 2.9 ± 2.6%). We conclude that (1) flow-mediated endothelium-dependent vasodilation in the brachial artery is impaired in patients with hypertension, (2) a relationship exists between the left ventricular mass index and flow-mediated endothelium-dependent vasodilation in the brachial artery in patients with hypertension and (3) increased oxidative stress may play a role in the endothelial dysfunction in patients with hypertension.

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“…Aortic and mesenteric arterial SMCs were isolated from wild-type and iPLA 2 ␤-null mice essentially using minor modifications of a previously described method (33,34). Briefly, to isolate mesenteric arterial SMCs, the subxiphoid abdominal region of asphyxiated mice (age 10 -14 weeks) was incised, and the mesenteric arcade was exposed.…”

Section: Methodsmentioning

confidence: 99%

Smooth Muscle Cell Arachidonic Acid Release, Migration, and Proliferation Are Markedly Attenuated in Mice Null for Calcium-independent Phospholipase A2β

Moon

Jenkins

Mancuso

et al. 2008

Journal of Biological Chemistry

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Pharmacologic evidence suggests that the lipid products generated by one or more calcium-independent phospholipases A 2 (iPLA 2 s) participate in the regulation of vascular tone through smooth muscle cell (SMC) Ca 2؉ signaling and the release of arachidonic acid. However, the recent identification of new members of the iPLA 2 family, each inhibitable by (E)-6-(bromomethylene)-3-(1-naphthalenyl)-2H-tetrahydropyran-2-one, has rendered definitive identification of the specific enzyme(s) mediating these processes difficult. Accordingly, we used iPLA 2 ␤ ؊/؊ mice to demonstrate that iPLA 2 ␤ is responsible for the majority of thapsigargin and ionophore (A23187)-induced arachidonic acid release from SMCs. Both thapsigargin and A23187 stimulated robust [ 3 H]arachidonate (AA) release from wild-type aortic SMCs that was dramatically attenuated in iPLA 2 ␤ ؊/؊ mice (>80% reduction at 5 min; p < 0.01). Moreover, iPLA 2 ␤ ؊/؊ mice displayed defects in SMC Ca 2؉ homeostasis and decreased SMC migration and proliferation in a model of vascular injury. Ca 2؉ -store depletion resulted in the rapid entry of external Ca 2؉ into wild-type aortic SMCs that was significantly slower in iPLA 2 ␤-null cells (p < 0.01). Furthermore, SMCs from iPLA 2 ␤-null mesenteric arterial explants demonstrated decreased proliferation and migration. The defects in migration and proliferation in iPLA 2 ␤-null SMCs were restored by 2 M AA. Remarkably, the cyclooxygenase-2-specific inhibitor, NS-398, prevented AA-induced rescue of SMC migration and proliferation in iPLA 2 ␤ ؊/؊ mice. Moreover, PGE 2 alone rescued proliferation and migration in iPLA 2 ␤ ؊/؊ mice. We conclude that iPLA 2 ␤ is an important mediator of AA release and prostaglandin E 2 production in SMCs, modulating vascular tone, cellular signaling, proliferation, and migration.Phospholipases A 2 (PLA 2 s) 2 catalyze hydrolysis of the sn-2 fatty acid substituent of glycerophospholipid substrates to yield a free fatty acid (e.g. arachidonic acid (AA)) and a 2-lysophospholipid as reviewed previously (1, 2). Both reaction products as well as their downstream metabolites possess potent biologic regulatory functions (3, 4). Thus, members of the PLA 2 family initiate dual signaling pathways emanating from a single hydrolytic reaction. For example, AA can be converted to multiple eicosanoid products (e.g. prostaglandins, thromboxanes, leukotrienes, and epoxytrienes) (3), whereas lysophospholipids alter membrane dynamics modulating the activity of many transmembrane enzymes, regulate the electrophysiologic properties of multiple ion channels, and serve as metabolic nodes in signaling pathways (e.g. production of 2-arachidonoyl glycerol or AA from 2-arachidonoyl lysophosphatidylcholine) (5, 6). Furthermore, both eicosanoids and lysolipids interact with a diverse array of cellular receptors further amplifying the repertoire of biologic responses initiated by phospholipase A 2 activity (7-9). Because many eicosanoids and lysolipids mediate alterations in vascular tone and inflammatory responses, the d...

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Culture of rat mesenteric arteriolar smooth muscle cells: effects of platelet-derived growth factor, angiotensin, and nitric oxide on growth

Cited by 29 publications

References 21 publications

Nitric oxide synthase and NAD(P)H oxidase modulate coronary endothelial cell growth

Nitric oxide synthase and NAD(P)H oxidase modulate coronary endothelial cell growth

The Relationship of Left Ventricular Mass to Endothelium-Dependent Vasodilation of the Brachial Artery in Patients with Hypertension

Smooth Muscle Cell Arachidonic Acid Release, Migration, and Proliferation Are Markedly Attenuated in Mice Null for Calcium-independent Phospholipase A2β

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