Expression of Endothelin-1, Endothelin-3, Endothelin-Converting Enzyme-1, and Endothelin-A and Endothelin-B Receptor mRNA After Angioplasty-Induced Neointimal Formation in the Rat

Wang, Xinkang; Douglas, Stephen A.; Louden, Calvert; Vickery-Clark, Lynne M.; Feuerstein, Giora; Ohlstein, Eliot H.

doi:10.1161/01.res.78.2.322

Cited by 135 publications

(75 citation statements)

References 34 publications

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“…Certainly, the transient perivascular inflammatory reaction 57 and ischemia of vasa vasorum 6,7 induced soon after endothelial injury may cause the release of a number of growth factors/cytokines, which may have a profound effect on the subsequent activation of local resident cells or blood-and SM-derived cells. Among the factors putatively involved, endothelin-1, 58,59 as demonstrated in this study ( Figure 6E and Table 2), transforming growth factor-␤1, 60 and platelet-derived growth factor 9 seem to be good candidates. It remains to be established whether and how the process of activation-recruitment-incorporation of adventitial cells in the media (and neointima) is operative during atherogenesis.…”

Section: Perspectivesmentioning

confidence: 56%

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

Faggin

Puato

Zardo

et al. 1999

ATVB

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Abstract-During the "response-to-injury" process after a mechanical insult to the porcine coronary arteries, the adventitial cells acquire the structural characteristics of myofibroblasts before being incorporated into smooth muscle (SM) layer.We assessed whether the SM-specific SM22 protein can be used as a tracer of adventitial cell-myofibroblast differentiation in the mild balloon injury of rabbit carotid artery. To achieve this goal, we used 2 monoclonal anti-SM22 antibodies (E-11 and 1-B8) and a molecular probe for the SM22␣ mRNA isoform in immunocytochemical and in situ hybridization experiments. The differentiation profile and the migratory and proliferative ability of activated adventitial cells were evaluated by a panel of antibodies to some SM and nonmuscle antigens and pulse-and end-labeling with bromo-deoxyuridine, respectively. In adventitial cells, SM22 antigenicity and SM22␣ mRNA were detectable at days 2 and 4 and, to a lesser extent, at days 7 and 21 after injury, particularly near the adventitia-media interface and mostly colocalizing with bromo-deoxyuridine-positive cells. The pulse-labeling experiments showed that the large majority of these cells penetrated the outermost layer of the tunica media without migrating to the subendothelial region. The phenotypic features of activated migrating and nonmigrating adventitial cells resembled those of vimentin-actin myofibroblast subtype and fetal-type SM cells. These findings indicate that a direct exposure of adventitia to the lumen is not required for phenotypic changes and proliferation/migration of these cells. After comparison of the SM22 expression in arterial vessels during early stages of development, we hypothesize that in the injured carotid artery the mural incorporation of adventitial cells and the spatiotemporal activation of SM22 expression are reminiscent of the vascular morphogenetic process and suggest the existence of a stem cell-like reservoir in adventitia. The early adventitial upregulation of SM22 expression in the injured vessel might be related to a multistep transition process in which nonmuscle cells are converted to myofibroblasts and, possibly, to SM cells. (Arterioscler Thromb Vasc Biol.

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Section: Perspectivesmentioning

confidence: 56%

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

Faggin

Puato

Zardo

et al. 1999

ATVB

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“…To define the optimal amplification cycle, pilot studies were performed using RT products from 0.3 µg of control RNA and 20 to 30 cycles of PCR amplification. 32 Because the amplified products for both NOS3 and ␤-actin during 24 to 30 cycles were represented as bands on the autoradiography and densitometric intensity of these bands was linearly increased, the amplification of 28 cycles was used in this study. The temperature profile of amplification was 94°C for 1 minute, 63°C for 1 minute, and 72°C for 2 minutes.…”

Section: Rna Isolation and Reverse Transcription-polymerase Chain Reamentioning

confidence: 99%

Tumor necrosis factor ? regulates nitric oxide synthase expression in portal hypertensive gastric mucosa of rats

et al. 1998

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Anti-tumor necrosis factor ␣ (TNF-␣) treatment decreases nitric oxide (NO) synthesis and ameliorates the hyperdynamic circulation in portal hypertensive rats. We have recently demonstrated that nitric oxide synthase isoform 3 (NOS3) is overexpressed in portal hypertensive gastric mucosa and that resultant NO overproduction probably is responsible for the increased susceptibility of the mucosa to damage. In the present study, we examined whether TNF-␣ is overexpressed in portal hypertensive gastric mucosa and whether anti-TNF-␣ treatment affects gastric NOS3 messenger RNA (mRNA) and protein expression. We examined plasma concentrations of TNF-␣ and its protein expression in gastric specimens from portal hypertensive and sham-operated rats using Western blotting and immunohistochemistry. We also measured gastric mucosal blood flow, gastric expression of NOS3 mRNA and protein, and NOS3 enzyme activity in rats with and without TNF-␣-neutralizing antibody treatment. The TNF-␣ protein levels in portal hypertensive stomachs were significantly increased by 57% compared with levels in sham-operated controls. TNF-␣ antibody treatment normalized gastric mucosal blood flow in portal hypertensive stomachs and significantly reversed overexpression of gastric NOS3 mRNA, protein, and its enzyme activity in portal hypertensive rats by 48%, 45%, and 33%, respectively. These results suggest that TNF-␣ may regulate NOS3 expression in the portal hypertensive stomach and that anti-TNF-␣ treatment may ameliorate the pathophysiological abnormalities of portal hypertensive gastric mucosa. (HEPATOLOGY 1998;27: 906-913.)Portal hypertensive (PHT) gastropathy is now recognized as a clinical entity that is frequently seen in patients with portal hypertension. 1-3 The PHT gastric mucosa has distinct morphological and functional abnormalities that increase its susceptibility to damage by noxious factors such as alcohol, aspirin, and ischemia/reperfusion. [4][5][6][7][8][9] We have recently showed that nitric oxide synthase isoform 3 (NOS3) messenger RNA (mRNA) and protein are overexpressed in PHT gastric mucosa of rats, and this overexpression may be, at least in part, responsible for the increased susceptibility of PHT gastric mucosa to damage. 10

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“…In angioplasty-induced neointima in rats, expressions of the mRNAs of endothelin-1, endothelin-3, ECE-1, ETA and ETB receptor were found to be increased (234). Cultured vascular smooth muscle cells explanted from human coronary artery were shown to secrete considerable amounts of endothelin-1 and big endothelin-1 (235).…”

Section: V-5 Vascular Thickeningmentioning

confidence: 97%

Molecular Pharmacology and Pathophysiological Significance of Endothelin

Goto

Hama

Kasuya

1996

Japanese Journal of Pharmacology

159

108

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ABSTRACT-Since the discovery of the most potent vasoconstrictor peptide, endothelin, in 1988, explosive investigations have rapidly clarified much of the basic pharmacological, biochemical and molecular biological features of endothelin, including the presence and structure of isopeptides and their genes (endothelin-1, -2 and -3), regulation of gene expression, intracellular processing, specific endothelia converting enzyme (ECE), receptor subtypes (ETA and ETB), intracellular signal transduction following receptor activation, etc. ECE was recently cloned, and its structure was shown to be a single transmembrane protein with a short intracellular N-terminal and a long extracellular C-terminal that contains the catalytic domain and numerous N-glycosylation sites. In addition to acute contractile or secretory actions, endothelin has been shown to exert long-term proliferative actions on many cell types. In this case, intracellular signal transduction appears to converge to activation of mitogen-activated protein kinase. As a recent dramatic advance, a number of non-peptide and orally active receptor antagonists have been developed. They, as well as current peptide antagonists, markedly accelerated the pace of investigations into the true pathophysiological roles of endogenous endothelin-1 in mature animals; e.g., hypertension, pulmonary hypertension, acute renal failure, cerebral vasospasm, vascular thickening, cardiac hypertrophy, chronic heart failure, etc. Thus, the interference with the endothelin pathway by either ECE-inhibition or receptor blockade may

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Expression of Endothelin-1, Endothelin-3, Endothelin-Converting Enzyme-1, and Endothelin-A and Endothelin-B Receptor mRNA After Angioplasty-Induced Neointimal Formation in the Rat

Cited by 135 publications

References 34 publications

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

Tumor necrosis factor ? regulates nitric oxide synthase expression in portal hypertensive gastric mucosa of rats

Molecular Pharmacology and Pathophysiological Significance of Endothelin

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