Angiotensin II induces plasminogen activator inhibitor-1 and -2 expression in vascular endothelial and smooth muscle cells.

Feener, Edward P.; Northrup, J M; Aiello, Lloyd Paul; King, George L.

doi:10.1172/jci117786

Cited by 252 publications

(154 citation statements)

References 56 publications

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“…Rat aortic smooth muscle cells (RASMCs) were isolated from SpragueDawley rats, cultured in Dulbecco's modified Eagle's medium (DMEM), 100 mg/dL D-glucose (Gibco-BRL), and 10% FBS (Gibco BRL) as described previously 23 and used between passages 8 and 15. Human aortic smooth muscle cells (HASMCs) were isolated from aortic …”

Section: Cell Culturementioning

confidence: 99%

“…The RNA was transferred to Biotrans membranes (ICN Pharmaceuticals) and cross-linked by UV. A cDNA probe against rat PAI-1 23 was labeled by using the Multiprime DNA labeling system (Amersham Corp) and purified with a NICK column (Pharmacia LKB Biotechnology Inc). A human PAI-1 antisense oligonucleotide (Oncogene Science Inc) was end-labeled by using T4 polynucleotide kinase and [ 32 P]ATP and then purified with a NAP-5 column (Pharmacia LKB).…”

Section: Rna Isolation and Northern Blot Analysismentioning

confidence: 99%

“…23 Conditioned media from RASMCs or HASMCs, treated with Ang II and PDGF in the absence or presence of ANF and CNP, was collected. Equal aliquots of conditioned media were separated by 10% SDS-polyacrylamide gel electrophoresis and transferred to nitrocellulose (Novex).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…[22][23][24] Control cells and cells pretreated with natriuretic factors for 5 minutes were stimulated with either Ang II or PDGF for 3 hours. Northern blot analyses of both PAI-1 and acidic ribosomal phosphoprotein PO mRNA (36B4, a constitutively expressed mRNA) were performed as described previously.…”

Section: Effect Of Natriuretic Peptides On Pai-1 Mrna Expression In Rmentioning

confidence: 99%

“…[22][23][24][25][26] However, although the processes that upregulate PAI-1 expression have received considerable attention, much less is known regarding the factors and mechanisms that may negatively regulate PAI-1 expression in vascular cells. In this report, we have examined the effect of 2 types of vasorelaxant compounds, natriuretic factors and nitric oxide, on the regulation of PAI-1 expression in VSMCs.…”

mentioning

confidence: 99%

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Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Bouchie

Hansen

Feener

1998

ATVB

105

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Abstract-Increased expression of plasminogen activator inhibitor-1 (PAI-1) has been reported in atherosclerotic and balloon-injured vessels. Little is known regarding the factors and mechanisms that may negatively regulate PAI-1 expression. In this report, the effect of cGMP-coupled vasoactive hormones, including natriuretic factors and nitric oxide, on the regulation of PAI-1 expression in vascular smooth muscle cells was examined. Atrial natriuretic factor 1-28 (ANF) and C-type natriuretic factor-22 (CNP) reduced angiotensin II (Ang II)-and platelet-derived growth factor-stimulated PAI-1 mRNA expression in rat aortic smooth muscle cells by 50% to 70%, with corresponding reductions in PAI-1 protein release. Treatment of human aortic smooth muscle cells with CNP similarly inhibited both platelet-derived growth factor-induced PAI-1 mRNA expression and PAI-1 protein release by 50%. Dose-response studies revealed that the inhibitory effects of CNP and ANF on PAI-1 expression were concentration dependent, with IC 50 s of Ϸ1 nmol/L for both natriuretic peptides. Ang II-stimulated PAI-1 expression was also inhibited by the nitric oxide donor S-nitroso-N-acetylpenicillamine.

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Section: Cell Culturementioning

confidence: 99%

Section: Rna Isolation and Northern Blot Analysismentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Effect Of Natriuretic Peptides On Pai-1 Mrna Expression In Rmentioning

confidence: 99%

mentioning

confidence: 99%

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Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Bouchie

Hansen

Feener

1998

ATVB

105

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Current Strategies for Management of Hypertensive Renal Disease

Moore¹,

Epstein²,

Agodoa³

et al. 1999

Arch Intern Med

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The incidence of hypertensive end-stage renal disease continues to increase annually. To reduce this incidence, it is necessary to control systolic and diastolic hypertension. Reversible causes should always be sought in any hypertensive patient who develops renal insufficiency. Blood pressure should be reduced to 130/85 mm Hg, and in African Americans with hypertensive renal failure, reducing the blood pressure to 120/75 mm Hg may be beneficial. Any antihypertensive treatment regimen that effectively lowers blood pressure will help slow progressive renal failure. Whenever possible, an angiotensin-converting enzyme inhibitor should be part of the treatment, since these drugs have been shown to be renoprotective beyond their antihypertensive effect in certain renal disease categories.

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Relationship between plasma plasminogen activator inhibitor 1 and insulin resistance

Bastard

Piéroni

Hainque

2000

Diabetes Metab. Res. Rev.

137

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High plasminogen activator inhibitor 1 (PAI-1) levels are associated with an increased cardiovascular risk of atherothrombosis. Furthermore, increased plasma PAI-1 levels are associated with dyslipidemia, hyperinsulinemia and hypertension. This association between PAI-1 and metabolic components of the Metabolic Syndrome could explain the predisposition of insulin resistant patients to atherothrombosis. Recent studies have suggested that visceral adipose tissue might be the link between elevated plasma PAI-1 and insulin resistance in the Metabolic Syndrome. Indeed, visceral adipose tissue was proposed as a potentially important source of PAI-1 in humans. However, in light of recent studies, visceral adipose tissue appears to be involved in the increase of plasma PAI-1 via the metabolic disorders usually associated with central obesity, rather than directly. High plasma PAI-1 levels are undoubtedly related to insulin resistance, and the mechanisms which could explain such an increase in the Metabolic Syndrome appear to be multi-factorial and remain to be elucidated. These mechanisms may involve several metabolic disorders such as hyperinsulinemia, dyslipidemia, impaired glucose tolerance and hypertension, which would favor PAI-1 synthesis and release from different cell types.

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Angiotensin II induces plasminogen activator inhibitor-1 and -2 expression in vascular endothelial and smooth muscle cells.

Abstract: Invest. 1995Invest. . 95:1353Invest. -1362

Cited by 252 publications

References 56 publications

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Current Strategies for Management of Hypertensive Renal Disease

Relationship between plasma plasminogen activator inhibitor 1 and insulin resistance

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