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Roles of Purinergic Receptor P2Y, G Protein–Coupled 12 in the Development of Atherosclerosis in Apolipoprotein E–Deficient Mice

OBJECTIVE—: The aim of the study was to evaluate the role of purinergic receptor P2Y, G protein–coupled 12 (P2Y12), an ADP receptor, in the development of atherosclerotic lesions. METHODS AND RESULTS—: Apolipoprotein E–null mice were crossed with P2y12 mice to generate double knockout mice. The doub... Full description

Journal Title: Arteriosclerosis Thrombosis, and Vascular Biology, 2012, Vol.32(8), pp.e81-e89
Main Author: Li, Kent, Ding
Other Authors: Wang, Kent, Yanhua , Zhang, Kent, Lin , Luo, Kent, Xinping , Li, Kent, Jian , Chen, Kent, Xuejin , Niu, Kent, Haixia , Wang, Kent, Kemin , Sun, Kent, Yueping , Wang, Kent, Xuefeng , Yan, Kent, Yan , Chai, Kent, Weiran , Gartner, Kent, T. , Liu, Kent, Junling
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ID: ISSN: 1079-5642 ; DOI: 10.1161/ATVBAHA.111.239095
Link: http://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00043605-201208000-00018
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title: Roles of Purinergic Receptor P2Y, G Protein–Coupled 12 in the Development of Atherosclerosis in Apolipoprotein E–Deficient Mice
format: Article
creator:
  • Li, Kent, Ding
  • Wang, Kent, Yanhua
  • Zhang, Kent, Lin
  • Luo, Kent, Xinping
  • Li, Kent, Jian
  • Chen, Kent, Xuejin
  • Niu, Kent, Haixia
  • Wang, Kent, Kemin
  • Sun, Kent, Yueping
  • Wang, Kent, Xuefeng
  • Yan, Kent, Yan
  • Chai, Kent, Weiran
  • Gartner, Kent, T.
  • Liu, Kent, Junling
subjects:
  • Medicine
ispartof: Arteriosclerosis, Thrombosis, and Vascular Biology, 2012, Vol.32(8), pp.e81-e89
description: OBJECTIVE—: The aim of the study was to evaluate the role of purinergic receptor P2Y, G protein–coupled 12 (P2Y12), an ADP receptor, in the development of atherosclerotic lesions. METHODS AND RESULTS—: Apolipoprotein E–null mice were crossed with P2y12 mice to generate double knockout mice. The double knockout mice and the control apolipoprotein E–null mice were fed a high-fat diet for 20 weeks. Assessment of the atherosclerotic lesions in the control and double knockout mice demonstrated that P2Y12 deficiency caused a diminished lesion area, an increased fibrous content at the plaque site, and decreased monocyte/macrophage infiltration of the lesions. Polymerase chain reaction studies revealed that white blood cells do not express significant levels of P2Y12. Bone marrow transplantation experiments confirmed that P2Y12 expressed on platelets is a key factor responsible for atherosclerosis, but do not exclude a role of smooth muscle cell P2Y12. Supernatant fluid from activated P2y12 but not P2y12 platelets was capable of causing monocyte migration. In vitro studies showed that platelet P2Y12 deficiency suppressed platelet factor 4 secretion and P-selectin expression. Further work demonstrated that platelet P2Y12, through inhibition of the cAMP/protein kinase A pathway, critically regulates the release of platelet factor 4, and thereby affects monocyte recruitment and infiltration. CONCLUSION—: These results demonstrate that P2Y12 modulates atherogenesis, at least in part by augmenting inflammatory cell recruitment via regulation of platelet α-granule release.
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identifier: ISSN: 1079-5642 ; DOI: 10.1161/ATVBAHA.111.239095
fulltext: fulltext
issn:
  • 1079-5642
  • 10795642
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titleRoles of Purinergic Receptor P2Y, G Protein–Coupled 12 in the Development of Atherosclerosis in Apolipoprotein E–Deficient Mice
creatorLi, Kent, Ding ; Wang, Kent, Yanhua ; Zhang, Kent, Lin ; Luo, Kent, Xinping ; Li, Kent, Jian ; Chen, Kent, Xuejin ; Niu, Kent, Haixia ; Wang, Kent, Kemin ; Sun, Kent, Yueping ; Wang, Kent, Xuefeng ; Yan, Kent, Yan ; Chai, Kent, Weiran ; Gartner, Kent, T. ; Liu, Kent, Junling
ispartofArteriosclerosis, Thrombosis, and Vascular Biology, 2012, Vol.32(8), pp.e81-e89
identifierISSN: 1079-5642 ; DOI: 10.1161/ATVBAHA.111.239095
descriptionOBJECTIVE—: The aim of the study was to evaluate the role of purinergic receptor P2Y, G protein–coupled 12 (P2Y12), an ADP receptor, in the development of atherosclerotic lesions. METHODS AND RESULTS—: Apolipoprotein E–null mice were crossed with P2y12 mice to generate double knockout mice. The double knockout mice and the control apolipoprotein E–null mice were fed a high-fat diet for 20 weeks. Assessment of the atherosclerotic lesions in the control and double knockout mice demonstrated that P2Y12 deficiency caused a diminished lesion area, an increased fibrous content at the plaque site, and decreased monocyte/macrophage infiltration of the lesions. Polymerase chain reaction studies revealed that white blood cells do not express significant levels of P2Y12. Bone marrow transplantation experiments confirmed that P2Y12 expressed on platelets is a key factor responsible for atherosclerosis, but do not exclude a role of smooth muscle cell P2Y12. Supernatant fluid from activated P2y12 but not P2y12 platelets was capable of causing monocyte migration. In vitro studies showed that platelet P2Y12 deficiency suppressed platelet factor 4 secretion and P-selectin expression. Further work demonstrated that platelet P2Y12, through inhibition of the cAMP/protein kinase A pathway, critically regulates the release of platelet factor 4, and thereby affects monocyte recruitment and infiltration. CONCLUSION—: These results demonstrate that P2Y12 modulates atherogenesis, at least in part by augmenting inflammatory cell recruitment via regulation of platelet α-granule release.
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titleRoles of Purinergic Receptor P2Y, G Protein–Coupled 12 in the Development of Atherosclerosis in Apolipoprotein E–Deficient Mice
descriptionOBJECTIVE—: The aim of the study was to evaluate the role of purinergic receptor P2Y, G protein–coupled 12 (P2Y12), an ADP receptor, in the development of atherosclerotic lesions. METHODS AND RESULTS—: Apolipoprotein E–null mice were crossed with P2y12 mice to generate double knockout mice. The double knockout mice and the control apolipoprotein E–null mice were fed a high-fat diet for 20 weeks. Assessment of the atherosclerotic lesions in the control and double knockout mice demonstrated that P2Y12 deficiency caused a diminished lesion area, an increased fibrous content at the plaque site, and decreased monocyte/macrophage infiltration of the lesions. Polymerase chain reaction studies revealed that white blood cells do not express significant levels of P2Y12. Bone marrow transplantation experiments confirmed that P2Y12 expressed on platelets is a key factor responsible for atherosclerosis, but do not exclude a role of smooth muscle cell P2Y12. Supernatant fluid from activated P2y12 but not P2y12 platelets was capable of causing monocyte migration. In vitro studies showed that platelet P2Y12 deficiency suppressed platelet factor 4 secretion and P-selectin expression. Further work demonstrated that platelet P2Y12, through inhibition of the cAMP/protein kinase A pathway, critically regulates the release of platelet factor 4, and thereby affects monocyte recruitment and infiltration. CONCLUSION—: These results demonstrate that P2Y12 modulates atherogenesis, at least in part by augmenting inflammatory cell recruitment via regulation of platelet α-granule release.
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authorLi, Kent, Ding ; Wang, Kent, Yanhua ; Zhang, Kent, Lin ; Luo, Kent, Xinping ; Li, Kent, Jian ; Chen, Kent, Xuejin ; Niu, Kent, Haixia ; Wang, Kent, Kemin ; Sun, Kent, Yueping ; Wang, Kent, Xuefeng ; Yan, Kent, Yan ; Chai, Kent, Weiran ; Gartner, Kent, T. ; Liu, Kent, Junling
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abstractOBJECTIVE—: The aim of the study was to evaluate the role of purinergic receptor P2Y, G protein–coupled 12 (P2Y12), an ADP receptor, in the development of atherosclerotic lesions. METHODS AND RESULTS—: Apolipoprotein E–null mice were crossed with P2y12 mice to generate double knockout mice. The double knockout mice and the control apolipoprotein E–null mice were fed a high-fat diet for 20 weeks. Assessment of the atherosclerotic lesions in the control and double knockout mice demonstrated that P2Y12 deficiency caused a diminished lesion area, an increased fibrous content at the plaque site, and decreased monocyte/macrophage infiltration of the lesions. Polymerase chain reaction studies revealed that white blood cells do not express significant levels of P2Y12. Bone marrow transplantation experiments confirmed that P2Y12 expressed on platelets is a key factor responsible for atherosclerosis, but do not exclude a role of smooth muscle cell P2Y12. Supernatant fluid from activated P2y12 but not P2y12 platelets was capable of causing monocyte migration. In vitro studies showed that platelet P2Y12 deficiency suppressed platelet factor 4 secretion and P-selectin expression. Further work demonstrated that platelet P2Y12, through inhibition of the cAMP/protein kinase A pathway, critically regulates the release of platelet factor 4, and thereby affects monocyte recruitment and infiltration. CONCLUSION—: These results demonstrate that P2Y12 modulates atherogenesis, at least in part by augmenting inflammatory cell recruitment via regulation of platelet α-granule release.
pub© 2012 American Heart Association, Inc.
doi10.1161/ATVBAHA.111.239095
eissn15244636
date2012-08