Ex Vivo Antisense Oligonucleotides to Proliferating Cell Nuclear Antigen and Cdc2 Kinase Inhibit Graft Coronary Artery Disease

Miniati, Douglas N.; Hoyt, E. Grant; Poston, Robert; Robbins, Robert C.

doi:10.1161/01.cir.102.suppl_3.iii-237

Cited by 17 publications

(18 citation statements)

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“…There was no statistically significant difference in these responses between the mutants. Increased immunohistochemical staining of α-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA) and tenascin-C (TN-C) in the mutant response to injury (Figure 4D) was consistent with VSMC proliferation and migration along the tenascin scaffold to form the neointima 26-28 .…”

Section: Resultsmentioning

confidence: 86%

Cell Selective Cardiovascular Biology of Microsomal Prostaglandin E Synthase-1

Chen

Yang

et al. 2013

Circulation

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Background Global deletion of microsomal prostaglandin E synthase (mPGES) -1 in mice attenuates the response to vascular injury without a predisposition to thrombogenesis or hypertension. However, enzyme deletion results in cell specific differential utilization by prostaglandin (PG) synthases of the accumulated PGH2 substrate. Here, we generated mice deficient in mPGES-1 in vascular smooth muscle cells (VSMCs), endothelial cells (ECs) and myeloid cells further to elucidate the cardiovascular function of this enzyme. Methods and Results VSMC and EC mPGES-1 deletion did not alter blood pressure at baseline or in response to a high salt diet. The propensity to evoked macrovascular and microvascular thrombogenesis was also unaltered. However, both VSMC and EC mPGES-1 deficient mice exhibited a markedly exaggerated neointimal hyperplastic response to wire injury of the femoral artery compared to their littermate controls. The hyperplasia was associated with increased proliferating cell nuclear antigen (PCNA) and tenascin-C (TN-C) expression. In contrast, the response to injury was markedly suppressed by myeloid cell depletion of mPGES-1 with decreased hyperplasia, leukocyte infiltration and expression of PCNA and TN-C. Conditioned medium derived from mPGES-1 deficient macrophages less potently induced VSMC proliferation and migration than that from wild type macrophages. Conclusion Deletion of mPGES-1 in the vasculature and myeloid cells differentially modulates the response to vascular injury, implicating macrophage mPGES-1 as a cardiovascular drug target.

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Section: Resultsmentioning

confidence: 86%

Cell Selective Cardiovascular Biology of Microsomal Prostaglandin E Synthase-1

Chen

Yang

et al. 2013

Circulation

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“…Therefore, the detection of PCNA expression in hyperplasia intima mainly reflected the proliferation of VSMC. It has been reported that the expression level of PCNA is linearly related to the cell proliferation (Miniati et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of aortic intimal hyperplasia and cell cycle protein and extracellular matrix protein expressions by BuYang HuanWu Decoction

Zhang

et al. 2009

Journal of Ethnopharmacology

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“…PCNA is a sensitive marker of cells in S phase of cell cycle. Previous studies have shown that the expression of PCNA was directly proportional with the degree of cell proliferation (Miniati et al, 2000). Protooncogene c-fos was involved in the process of cell growth and differentiation and enabled cells to enter into the cell cycle from G 0 phase (Petkova et al, 2000).…”

Section: The Effects Of Byhwd and Its Effective Components On Vsmc Prmentioning

confidence: 99%

The effects of BuYang HuanWu Decoction and its effective components on proliferation-related factors and ERK1/2 signal transduction pathway in cultured vascular smooth muscle cells

Chen

Deng

2011

Journal of Ethnopharmacology

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Ex Vivo Antisense Oligonucleotides to Proliferating Cell Nuclear Antigen and Cdc2 Kinase Inhibit Graft Coronary Artery Disease

Cited by 17 publications

References 1 publication

Cell Selective Cardiovascular Biology of Microsomal Prostaglandin E Synthase-1

Cell Selective Cardiovascular Biology of Microsomal Prostaglandin E Synthase-1

Inhibition of aortic intimal hyperplasia and cell cycle protein and extracellular matrix protein expressions by BuYang HuanWu Decoction

The effects of BuYang HuanWu Decoction and its effective components on proliferation-related factors and ERK1/2 signal transduction pathway in cultured vascular smooth muscle cells

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