Reduction in the extent of atherosclerosis in apolipoprotein E-deficient mice induced by electroporation-mediated transfer of the human plasma platelet-activating factor acetylhydrolase gene into skeletal muscle

Hase, Makoto; Tanaka, Masashi; Yokota, Mitsuhiro; Yamada, Yoshiji

doi:10.1016/s0090-6980(02)00015-1

Cited by 38 publications

(14 citation statements)

References 22 publications

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“…75,76 The reduction of atherosclerotic lesions was more pronounced in male than in female mice and paralleled the level of Lp-PLA 2 activity after gene transfer. 77 In a model of postangioplasty restenosis in cholesterol-fed rabbits, adenovirus-mediated Lp-PLA 2 gene transfer reduced neointima formation in aorta.…”

Section: Pla 2 S and Experimental Atherosclerosismentioning

confidence: 85%

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease

2010

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Section: Pla 2 S and Experimental Atherosclerosismentioning

confidence: 85%

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease

2010

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“…The secreted or plasma form of PAF AH circulates in blood as a complex with lipoproteins (7). Its precise role in pathophysiological processes is controversial (8 -14) but our work and that of others has shown that the enzyme has anti-inflammatory properties in vivo (15)(16)(17)(18)(19)(20).…”

mentioning

confidence: 86%

The p38 MAPK Pathway Mediates Transcriptional Activation of the Plasma Platelet-activating Factor Acetylhydrolase Gene in Macrophages Stimulated with Lipopolysaccharide

Zimmerman

Prescott

et al. 2004

Journal of Biological Chemistry

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Administration of lipopolysaccharide (LPS) to experimental animals results in the up-regulation of expression of the plasma form of platelet-activating factor acetylhydrolase (PAF AH) in tissue macrophages. To investigate the mechanism underlying induction of PAF AH by LPS we used murine RAW264.7 and human THP-1 macrophages as model systems. We found that the p38 mitogen-activated protein kinase (p38 MAPK) pathway mediates transcriptional activation of the PAF AH gene through the participation of nucleotides ؊68/؊316 relative to the transcriptional initiation site. This promoter region spans two Sp1/Sp3 binding sites (SP-A and SP-B) and is necessary and sufficient for the observed effect. Disruption of these Sp binding sites significantly reduces promoter activity in LPS-stimulated cells. The ability of LPS to induce transcriptional activation of PAF AH is not due to enhanced Sp1/Sp3 binding to the promoter but involves enhanced transactivation function of Sp1 via p38 MAPK activation. These studies characterize the mechanism by which LPS modulates expression of PAF AH at the transcriptional level, and they have important implications for our understanding of responses that occur during the development of LPSmediated inflammatory diseases.

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“…Importantly, these beneficial changes occurred without decreasing the hypercholesteremia of these animals, showing that inflammatory events, and not the amount of circulating lipids, underlies disease progression. Electroporation of the plasma PAF-AH gene into muscle also increases circulating enzyme levels and reduces the mean thickness of the aortic wall in atherosclerosis-prone apoE-null mice (32).…”

Section: Inflammationmentioning

confidence: 97%

The emerging roles of PAF acetylhydrolase

McIntyre

Prescott

Stafforini

2009

Journal of Lipid Research

154

119

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Platelet-activating factor (PAF), a phospholipid autacoid with potent effects throughout the innate immune system, is selectively degraded by two small families of PAF acetylhydrolases (PAF-AHs). These Ca 21 -independent phospholipases A 2 display remarkable specificity for the length of the sn -2 residue, but this selectivity is lost as the residue gains oxygen functions. Two of the PAF-AHs therefore are specific oxidized phospholipid phospholipases that reduce inflammation, but also remove oxidatively truncated phospholipids that induce apoptosis. The roles of these enzymes are manifold, and their separate and combined functions are now being addressed in model systems and clinical studies-McIntyre, T. M., S. M. Prescott, and D. M. Stafforini. The emerging roles of PAF acetylhydrolase.

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Reduction in the extent of atherosclerosis in apolipoprotein E-deficient mice induced by electroporation-mediated transfer of the human plasma platelet-activating factor acetylhydrolase gene into skeletal muscle

Cited by 38 publications

References 22 publications

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease

The p38 MAPK Pathway Mediates Transcriptional Activation of the Plasma Platelet-activating Factor Acetylhydrolase Gene in Macrophages Stimulated with Lipopolysaccharide

The emerging roles of PAF acetylhydrolase

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Reduction in the extent of atherosclerosis in apolipoprotein E-deficient mice induced by electroporation-mediated transfer of the human plasma platelet-activating factor acetylhydrolase gene into skeletal muscle

Cited by 38 publications

References 22 publications

Lipoprotein-Associated and Secreted Phospholipases A 2 in Cardiovascular Disease

Lipoprotein-Associated and Secreted Phospholipases A 2 in Cardiovascular Disease

The p38 MAPK Pathway Mediates Transcriptional Activation of the Plasma Platelet-activating Factor Acetylhydrolase Gene in Macrophages Stimulated with Lipopolysaccharide

The emerging roles of PAF acetylhydrolase

Contact Info

Product

Resources

About

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease

Lipoprotein-Associated and Secreted Phospholipases A ₂ in Cardiovascular Disease