Nucleotide receptor P2y13

2005 ◽  
Author(s):  
Didier Communi ◽  
Frédéric Marteau ◽  
Abduelhakem Ben Addi ◽  
Nathalie Suarez Gonzalez ◽  
Bernard Robaye ◽  
...  
Keyword(s):  
Nucleotide Receptor

Nucleotide receptor P2x4

2006 ◽  
Author(s):  
Xuenong Bo ◽  
Geoff Burnstock ◽  
Bruce Liang
Keyword(s):  
Nucleotide Receptor

scholarly journals Agonist-induced phosphorylation and desensitization of the P2Y2 nucleotide receptor

2005 ◽  
Vol 280 (1-2) ◽  
pp. 35-45 ◽  
Author(s):  
Rosa V. Flores ◽  
Melvin G. Hernández-Pérez ◽  
Edna Aquino ◽  
Richard C. Garrad ◽  
Gary A. Weisman ◽  
...  
Keyword(s):  
Nucleotide Receptor

Nucleotide Receptor P2x

2012 ◽  
pp. 1275-1287
Author(s):  
Rüdiger Horstkorte ◽  
Bettina Büttner ◽  
Kaya Bork ◽  
Navdeep Sahota ◽  
Sarah Sabir ◽  
...  
Keyword(s):  
Nucleotide Receptor

scholarly journals Modulation of Neutrophil Apoptosis by Antimicrobial Peptides

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Isao Nagaoka ◽  
Kaori Suzuki ◽  
François Niyonsaba ◽  
Hiroshi Tamura ◽  
Michimasa Hirata
Keyword(s):  
Antimicrobial Peptides ◽  
Host Defense ◽  
Cell Activation ◽  
Immune Cell ◽  
Formyl Peptide Receptor ◽  
Bacterial Invasion ◽  
Neutrophil Apoptosis ◽  
Peptide Antibiotics ◽  
Nucleotide Receptor ◽  
Chemokine Production

Peptide antibiotics possess the potent antimicrobial activities against invading microorganisms and contribute to the innate host defense. Human antimicrobial peptides, α-defensins (human neutrophil peptides, HNPs), human β-defensins (hBDs), and cathelicidin (LL-37) not only exhibit potent bactericidal activities against Gram-negative and Gram-positive bacteria, but also function as immunomodulatory molecules by inducing cytokine and chemokine production, and inflammatory and immune cell activation. Neutrophil is a critical effector cell in host defense against microbial infection, and its lifespan is regulated by various pathogen- and host-derived substances. Here, we provided the evidence that HNP-1, hBD-3, and LL-37 cannot only destroy bacteria but also potently modulate (suppress) neutrophil apoptosis, accompanied with the phosphorylation of ERK-1/-2, the downregulation of tBid (an proapoptotic protein) and upregulation of Bcl-xL (an antiapoptotic protein), and the inhibition of mitochondrial membrane potential change and caspase 3 activity, possibly via the actions on the distinct receptors, the P2Y6 nucleotide receptor, the chemokine receptor CCR6, and the low-affinity formyl-peptide receptor FPRL1/the nucleotide receptor P2X7, respectively. Suppression of neutrophil apoptosis results in the prolongation of their lifespan and may be advantageous for the host defense against bacterial invasion.

Abstract 5543: The P2Y 2 Nucleotide Receptor Contributes To Intimal Lesion Growth And Regulates Lymphotoxin-α Secretion

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Gary Weisman ◽  
Ningpu Yu ◽  
Cansu Agca ◽  
Rikka Shivaji ◽  
Ying Wan ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Actin Binding ◽  
Dependent Manner ◽  
Filamin A ◽  
Nucleotide Receptor ◽  
Transgenic Rats ◽  
Arterial Lumen ◽  
Lesion Growth ◽  
Lymphotoxin Α ◽  
Intimal Lesion

Inflammatory processes play a crucial role in atherosclerotic lesion growth. A number of pro-inflammatory molecules have been implicated in the pathogenesis of atherosclerosis, including lymphotoxin-α (LTA). Our research has shown that activation of a G protein-coupled P2Y 2 nucleotide receptor (P2Y 2 R) expressed in vascular cells mediates inflammatory responses. To examine the role of the P2Y 2 R in lesion growth, we developed P2Y 2 R over-expressing transgenic rats. Collar-induced injury to the carotid artery of P2Y 2 R transgenic rats caused a dramatic increase in intimal lesion growth and significant macrophage accumulation, which nearly blocked the arterial lumen. Immunohistochemical staining showed that LTA and galectin-2 (gal-2) were abundantly expressed in smooth muscle cells (SMC) and macrophages in carotid lesions of P2Y 2 R transgenic rats. We also identified galectin-2 as a P2Y 2 R binding partner using the yeast two-hybrid system and a co-immunoprecipitation assay. P2Y 2 R agonist, UTP, stimulated gal-2 mRNA expression in rat carotid SMC. Transient transfection of SMC with a genomic fragment including the rat galectin (LGALS2) promoter incorporated into a luciferase (pGL-3) reporter vector showed that UTP markedly increased LGALS2 promoter activity in a dose-dependent manner. Moreover, UTP induced LTA secretion in cultured aortic SMC from wild type, but not P2Y 2 R −/− mice. Adenoviral expression of the full length P2Y 2 R in SMC from P2Y 2 R −/− mice fully restored UTP-induced LTA secretion. However, expression of a mutant P2Y 2 R that does not bind filamin A, an actin-binding protein that interacts with the P2Y 2 R, only partially restored UTP-induced LTA secretion in P2Y 2 R −/− SMC. Gal-2 siRNA partially inhibited LTA release into medium of cultured SMC expressing the P2Y 2 R. In contrast, gal-2 siRNA abolished UTP-induced LTA secretion in SMC isolated from P2Y 2 R −/− mice expressing the filamin A binding mutant P2Y 2 R. These results indicate that P2Y 2 Rs regulate gal-2-dependent LTA secretion in SMC via a filamin A-dependent mechanism that likely contributes to vascular inflammation.

Molecular cloning and characterization of the mouse P2Y4 nucleotide receptor

2001 ◽  
Vol 416 (3) ◽  
pp. 197-202 ◽  
Author(s):  
Nathalie Suarez-Huerta ◽  
Valérie Pouillon ◽  
Jean-Marie Boeynaems ◽  
Bernard Robaye
Keyword(s):  
Molecular Cloning ◽  
Nucleotide Receptor
Sign in / Sign up

Export Citation Format

Share Document