Increased release of ATP from endothelial cells during acute inflammation

Bodin, Philippe; Burnstock, Geoffrey

doi:10.1007/s000110050341

Cited by 165 publications

(120 citation statements)

References 23 publications

(32 reference statements)

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“…It has been shown that P2 activation leads to increases in concentration of intracellular calcium and PGE2 release (Naemsch et al, 2001). ATP, which activates this pathway, is typically released by bone, endothelial and epithelial cells and fibroblasts under stress conditions, acting as a DAMP/alarmin (Bodin & Burnstock, 1998;Burnstock, 1999;Furuya, Sokabe & Furuya, 2005;Grygorczyk & Hanrahan, 1997;John & Barakat, 2001;Katsuragi & Migita, 2004;Katz, Boland & Santillan, 2006;Kerkweg & de Groot, 2005;Milner et al, 1992;Milner et al, 1990b;Ohata et al, 1997;Patel et al, 2005;Romanello et al, 2001;Sauer, Hescheler & Wartenberg, 2000;Yamamoto et al, 2003).…”

Section: P2x7 Receptor: a Possible Mediator Of Orthodontic Mechanotramentioning

confidence: 99%

“…It can be activated (opened) after binding to extracellular ATP, which is a danger signal from cells under mechanical stress (Bodin & Burnstock, 1998;Milner et al, 1990a;Schneider et al, 2006). Opening of the channel causes the accumulation of intracellular calcium and the release of inflammatory mediators such as PGE2, IL-1α and IL-1β, all fundamental in the control of bone physiology (Brough et al, 2003;Ferrari et al, 2006;Gudipaty et al, 2003;Li et al, 2005;Lister et al, 2007).…”

Section: Orthodontic Mechanotransduction and The Role Of The P2x7 Recmentioning

confidence: 99%

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Orthodontic mechanotransduction and the role of the P2X7 receptor

Viecilli

Katona

Chen

et al. 2009

American Journal of Orthodontics and Dentofacial Orthopedics

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DEDICATIONTo my parents, who have supported my education. iv ACKNOWLEDGMENTSOne of the most important things I have learned during my PhD is the necessity of the existence of a working network of people that can help you achieve your goals. The more effectively this network functions, the higher the chance you will achieve the goals quickly.I would first like to thank my parents, who have unconditionally supported my decision to abandon a profitable private practice in Orthodontics, and return to humble student conditions while aiming for a full time academic career.I also thank my girlfriend Laura Kruter who has (almost always) been ok with my, some might say, not very sane ideas. Sometimes they do turn out fine, though (like this "PhD" one).I can hardly think of anyone else that could have complemented my work and ideas during this Program as well as Dr. Thomas Katona. While I was passionately conditioned to an idea, he was always rational and careful. While I was sometimes furious with a shortcoming, he was always temperate and humorous. When I ran into his office with some news about a project, he would always listen and almost never seem too busy to see me. While I was working and something went wrong, he would listen and wonder with me about the "whys" and "hows", instead of telling me what to do or express disappointment. He was even subject to some of my home culinary experiments. I was extremely fortunate to find someone that thought about science the same way I did, and that actually helped me with my project instead of just telling me what to do. I felt like we worked as a team, and that helped to increase my motivation during my studies. The third part of this project tested the role of the P2X7 receptor in the dentoalveolar morphology of C57B/6 mice. P2X7R KO (knockout) mice were compared to C57B/6 WT to identify differences in a maxillary molar and bone. Tooth dimensions viii were measured and 3D bone morphometry was conducted. No statistically significant differences were found between the two mouse types. P2X7R does not have a major effect on alveolar bone or tooth morphology.The final part examines the role of the P2X7 receptor in a controlled biomechanical model. Orthodontic mechanotransduction was compared in wild-type (WT) and P2X7R knock-out (KO) mice. Using Finite Element Analysis, mouse mechanics were scaled to produce typical human stress levels. Relationships between the biological responses and the calculated stresses were statistically tested and compared.There were direct relationships between certain stress magnitudes and root resorption and bone formation. Hyalinization and root and bone resorption were different in WT and KO. Orthodontic responses are related to the principal stress patterns in the PDL and the P2X7 receptor plays a significant role in their mechanotransduction.

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Section: P2x7 Receptor: a Possible Mediator Of Orthodontic Mechanotramentioning

confidence: 99%

Section: Orthodontic Mechanotransduction and The Role Of The P2x7 Recmentioning

confidence: 99%

Orthodontic mechanotransduction and the role of the P2X7 receptor

Viecilli

Katona

Chen

et al. 2009

American Journal of Orthodontics and Dentofacial Orthopedics

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“…Due to its size and high density of charge, ATP cannot permeate membranes. However, release of ATP has been observed from a variety of cells, including tumor cells and lymphocytes, as well as from virtually all tissues under conditions of hypoxia, ischemia, inflammation, and cell necrosis (5)(6)(7)(8). The sources of released ATP include exocytotic granula from secretory cells, release from lysed cells, and nonlytic release from cytoplasmatic stores.…”

Section: Endritic Cells (Dc)mentioning

confidence: 99%

Extracellular ATP and TNF-α Synergize in the Activation and Maturation of Human Dendritic Cells

Schnurr

Then

Galambos

et al. 2000

The Journal of Immunology

173

140

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Extracellular ATP mediates numerous biological activities by interacting with plasma membrane P2 purinergic receptors. Recently, P2 receptors have been described on dendritic cells (DC), but their functional role remains unclear. Proposed functions include improved Ag presentation, cytokine production, chemotaxis, and induction of apoptosis. We investigated the effects of ATP and of other P2 receptor agonists on endocytosis, phenotype, IL-12 secretion, and T cell stimulatory capacity of human monocyte-derived DC. We found that in the presence of extracellular ATP, DC transiently increase their endocytotic activity. Subsequently, DC up-regulate CD86, CD54, and MHC-II; secrete IL-12; and exhibit an improved stimulatory capacity for allogeneic T cells. These effects were more pronounced when chemically modified ATP derivatives with agonistic activity on P2 receptors, which are resistent to degradation by ectonucleotidases, were applied. Furthermore, ATP and TNF-α synergized in the activation of DC. Stimulated with a combination of ATP and TNF-α, DC expressed the maturation marker CD83, secreted large amounts of IL-12, and were potent stimulators of T cells. In the presence of the P2 receptor antagonist suramin, the effects of ATP were completely abolished. Our results suggest that extracellular ATP may play an important immunomodulatory role by activating DC and by skewing the immune reaction toward a Th1 response through the induction of IL-12 secretion.

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“…ATP can be released from endothelium in response to increases in shear stress (Bodin et al, 1991) and from perivascular nerve terminals (Ralevic & Burnstock, 1998;Burnstock & Kennedy, 1986). In¯ammatory mediators, ischaemia, and damage to blood vessels also cause ATP release from endothelial cells, neutrophils, cardiomyocytes, erythrocytes and platelets (Borst & Schrader, 1991;Born & Kratzer, 1984;Bodin & Burnstock, 1998;Pearson & Gordon, 1985;Yang et al, 1994;Bergfeld & Forrester, 1992;Gordon, 1986;Ralevic & Burnstock, 1991;1998;Sprague et al, 1996;Olsson & Pearson, 1990). ATP is rapidly broken down to adenosine by endothelial ectonucleotidases (Pearson & Gordon, 1985).…”

Section: Introductionmentioning

confidence: 99%

Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

Erga

Seubert

Liang

et al. 2000

British J Pharmacology

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1 Adenosine-5'-triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P 2 receptor activation or by A 2A -adenosine receptor activation. 2 E ects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea-pig isolated hearts perfused at a constant¯ow of 10 ml min 71 . 3 ATP and adenosine both caused sustained, concentration-dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD 2 (+s.e.mean) for ATP and adenosine were 6.68+0.04 and 7.06+0.05, respectively. Adenosine was signi®cantly more potent than ATP (P50.0001, n=10).4 The values of pIC 50 for the selective A 2A -adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28+0.08 and 8.28+0.06 (P=0.99, n=6), respectively. 5 The non-selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC 50 values 7.48+0.04 and 7.45+0.06, respectively) and adenosine (pIC 50 values 7.37+0.13 and 7.56+0.11). 6 In contrast to ATP and adenosine, the two P 2 agonists 2-methylthio-ATP and uridine-5'-triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8-parasulphophenyltheophylline, or XAC. 7 Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2-methylthio-ATP.

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Increased release of ATP from endothelial cells during acute inflammation

Abstract: These results show that non-damaged endothelial cells release ATP under experimental inflammatory conditions and support an early role of extracellular ATP in the inflammatory process.

Cited by 165 publications

References 23 publications

Orthodontic mechanotransduction and the role of the P2X7 receptor

Orthodontic mechanotransduction and the role of the P2X7 receptor

Extracellular ATP and TNF-α Synergize in the Activation and Maturation of Human Dendritic Cells

Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

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Increased release of ATP from endothelial cells during acute inflammation

Abstract: These results show that non-damaged endothelial cells release ATP under experimental inflammatory conditions and support an early role of extracellular ATP in the inflammatory process.

Cited by 165 publications

References 23 publications

Orthodontic mechanotransduction and the role of the P2X7 receptor

Orthodontic mechanotransduction and the role of the P2X7 receptor

Extracellular ATP and TNF-α Synergize in the Activation and Maturation of Human Dendritic Cells

Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

Contact Info

Product

Resources

About

Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart