Serum lipids and restenosis after successful percutaneous transluminal coronary angioplasty

Roth, Arie; Eshchar, Y; Keren, Gad; Sheps, David S.; Kerbel, Shimon; Laniado, Shlomo; Miller, Hylton I.; Rubinstein, Ardon

doi:10.1016/0002-9149(94)90173-2

Cited by 18 publications

(8 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The degree of hyperplasia was similar in mice fed low-or high-fat diets despite large lipoprotein differences between the two groups, a result consistent with human studies showing no association of plasma lipids and restenosis. 15 Restenosis studies in rat and mouse models are criticized for being conducted in normal arteries, whereas human restenosis occurs in atherosclerotic arteries. In part, this problem can be solved by either feeding mice with a high fat diet for a period of time long enough to induce significant atherosclerosis, or by using Apoe-or Ldlr-targeted mutant mice, both of which develop spontaneous atherosclerosis.…”

Section: See Page 955mentioning

confidence: 99%

Comparative Genetics of Atherosclerosis and Restenosis: Exploration With Mouse Models

Wang

Paigen

2002

ATVB

View full text Add to dashboard Cite

Section: See Page 955mentioning

confidence: 99%

Comparative Genetics of Atherosclerosis and Restenosis: Exploration With Mouse Models

Wang

Paigen

2002

ATVB

View full text Add to dashboard Cite

“…Restenosis is an occlusive vascular lesion characterized by the abnormal proliferation, migration and accumulation of media‐derived vascular smooth muscle cells (VSMC) within the arterial intima (‘neointima’). Within 3–12 months of mechanical injury to the vessel wall, 30–55% of patients treated surgically for atherosclerosis undergo symptomatic restenosis 1 , 2 , 3 . Although VSMC proliferation in response to injury‐related mitogens might be a major contributor to lesion formation, studies now indicate that during both atherosclerosis and restenosis, abnormal accumulation or loss of VSMC are due to an imbalance in cell proliferation versus cell death by apoptosis 3 , 4 , 5 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Evidence that insulin‐like growth factor‐1 requires protein kinase C‐ɛ, PI3‐kinase and mitogen‐activated protein kinase pathways to protect human vascular smooth muscle cells from apoptosis

et al. 2005

View full text Add to dashboard Cite

Summary Insulin-like growth factor (IGF)-1 has been implicated in the development of occlusive vascular lesions. Although its role in vascular smooth muscle cell (VSMC) growth and migration are fairly well characterized, antiapoptotic signals of IGF-1 in human VSMC remain largely unknown. In this study, we examined IGF-1 signals that protect human and rat VSMC from staurosporine (STAU)-and c-myc -induced apoptosis, respectively. Treatment with STAU resulted in apoptotic DNA fragmentation, phosphatidylserine externalization and cell shrinkage, but only occasional VSMC 'blebbing'. STAU-induced death and IGF-1-mediated survival were concentration dependent, while time-lapse video microscopy showed that IGF-1 inhibited c-myc -induced apoptosis by 90%. Pretreatment with mitogen-activated protein kinase/extracellular signal regulated kinase kinase (MEK) inhibitors UO126 and PD098059, or with the phosphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin, reversed IGF-1-mediated human VSMC survival by 25-27% and 66%, respectively. Translocation studies showed that IGF-1 activated protein kinase C (PKC)-ε , but not PKC-α or PKC-δ , even in the presence of STAU, while pharmacological PKC inhibition (Ro-318220 or Go6976) implicated PKC-ζ or a novel PKC isozyme in IGF-1-mediated survival. Transient expression of activated PKC-ε but not activated PKC-ζ decreased myc -induced apoptosis in rat VSMC. In human VSMC, antisense oligodeoxynucleotides to PKC-ε partially reversed IGF-1-induced survival. In addition, IGF-1 elicited a mild but sustained activation of extracellular signal regulated kinase (ERK)1/2 in human VSMC that was abolished after 1 h in the presence of STAU. PKC downregulation reversed both IGF-1-and PMA-induced ERK activity, but platelet-derived growth factor (PDGF)-induced activity was unchanged. These results indicate for the first time that IGF-1 can protect human VSMC via multiple signals, including PKC-ε , PI3-K and mitogenactivated protein kinase pathways.

show abstract

“…Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is a common and clinically important pathological complication [1,2]. Several studies have shown an adverse relation between elevated plasma lipids and endothelial healing process [3,4]. To date, there is inconsistent evidence supporting these parameters as a risk predictor of restenosis [3,5–7].…”

Section: Introductionmentioning

confidence: 99%

Lipid metabolism and occurrence of post-percutaneous transluminal coronary angioplasty restenosis: role of cholesteryl ester transfer protein and paraoxonase/arylesterase

Zee

Fernandez-Otiz

Macaya

et al. 2003

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

Summary. Plasma lipid metabolic and transfer processes have recently been suggested to play an important role in the development of early restenosis, a major complication of percutaneous transluminal coronary angioplasty (PTCA); in particular, the common variants of genes for cholesteryl ester transfer protein (CETP) and paraoxonase (PONA) have been implicated. We had the opportunity to investigate this question in a large, prospective cohort characterized by quantitative coronary angiography in all subjects. The CETP-TaqIB (intron 1), CETPMspI (intron 8), and PONA-AlwI (exon 2) polymorphisms were characterized in a cohort of 779 patients of whom 342 ('cases') had developed restenosis (as defined by >50% loss of lumen compared with immediate postprocedure results) at repeat angiography at 6 months post PTCA. Selected frequencies for CETP B1 and B2 alleles (absence/presence of TaqIB site) were 0.65 and 0.35 (cases) and 0.65 and 0.35 (controls), respectively; frequencies for CETP M1 and M2 alleles (absence/presence of MspI site) were 0.20 and 0.80 (cases), 0.21 and 0.79 (controls), respectively; frequencies for PONA A and B alleles (absence/presence of AlwI site) were 0.73 and 0.27 (cases), 0.72 and 0.28 (controls), respectively. All observed genotype frequencies were in Hardy-Weinberg equilibrium. There was no evidence for gene-gene interaction, or an association between genotype and restenosis or degree of lumen loss (adjusted for covariates). Our data, collected in the largest study of its kind so far, indicate that the common variants for CETP and PONA are not associated with incidence of restenosis after PTCA, and are therefore not useful markers for risk assessment.

show abstract

Serum lipids and restenosis after successful percutaneous transluminal coronary angioplasty

Cited by 18 publications

References 23 publications

Comparative Genetics of Atherosclerosis and Restenosis: Exploration With Mouse Models

Comparative Genetics of Atherosclerosis and Restenosis: Exploration With Mouse Models

Evidence that insulin‐like growth factor‐1 requires protein kinase C‐ɛ, PI3‐kinase and mitogen‐activated protein kinase pathways to protect human vascular smooth muscle cells from apoptosis

Lipid metabolism and occurrence of post-percutaneous transluminal coronary angioplasty restenosis: role of cholesteryl ester transfer protein and paraoxonase/arylesterase

Contact Info

Product

Resources

About