Table 1.
Key Publications Describing ATP Release Mechanisms during Inflammation.
| Selected Reading | Type | Cells | Mechanisms | |||
|---|---|---|---|---|---|---|
| First Author | Last Author | Journal | Year | |||
| Kato, Y. | Miyaji, T. | PNAS | 2017 | Exocytosis | Neurons, microglia, immune cells | Reduction of neuropathic and inflammatory pain by clodronate (inhibitor of exocytosis) in mice [21] |
| Parzych, K. | Paul-Clark, M.J. | FASEB | 2017 | Pannexin-1 | THP-1 cells | IL1 β secretion from monocytes upon TLR2 stimulation is dependent on pannexin-1/ATP/P2X7 axis [22] |
| Saez, P.J. | Saez, J.C. | SCI SIGNAL | 2017 | Pannexin-1 | Dendritic cells | Dendritic cells release ATP via PANX1 hemichannels in response to ATP-dependent P2X7 activation. Released ATP amplifies DCs activation in autocrine manner [23] |
| Wang, X. | Sun, B. | PNAS | 2017 | Connexin 43 | dHL-60 | Neutrophils release ATP via CX43 in response to LPS stimulation. MLCK is activated and phosphorylates MLC, leading to chemotaxis stoppage [24] |
| Zhang, C. | Du, B. | J IMMUNOL | 2017 | Exocytosis + pannexin-1 | RAW 264.7 cells/293 T cells | ATP is released by virus infected macrophages and protects cells-limiting virus replication-via P2X7 and increased IFNgamma production [25] |
| Brown, I.A. | Gulbransen, B.D. | CELL MOL GASTROENTEROL HEPATOL | 2016 | Connexin 43 | Enteric glia | Upon oxidative stress, enteric glia release ATP via CX43. This mechanism is potentiated by NO. ATP further activates P2X7 leading to neuron death [26] |
| Qin, J. | Du, B. | J IMMUNOL | 2016 | Connexin 43 | RAW 264.7 | TLRs induce increased CX43 expression in macrophages and UDP release. UDP interacts with P2Y6 receptor and induces MCP-1 release [27] |
| Lim To, W.K. | Marshall, J.M. | PLACENTA | 2015 | Exocytosis | Endothelial cells (HUVEC) | Hypoxia induces ATP release which leads to vasodilation via an increased synthesis of PGs and NO [28] |
| Lohman, A.W. | Isakson, B.E. | NAT COMMUN | 2015 | Pannexin-1 | Endothelial cells (HUVEC) | TNF α released upon inflammation induces ATP release from vascular endothelial cells via PANX1 [29] |
| Chen, Y. | Junger, W.G. | SHOCK | 2015 | Pannexin-1 | PMNs | Hypertonic saline reduces PMNs overactivation by inducing ATP release via PANX1 channels. ATP is degraded to adenosine that interacts with A2a receptors on PMNs [30] |
| Yang, D. | Núñez, G. | IMMUNITY | 2015 | Pannexin-1 | BMMφ | Intracellular LPS activated caspase-11 cleaves PANX1 which releases ATP. ATP further activates P2X7 receptors ending with pyroptosis [31] |
| Molica, F. | Kwak, B.R. | J THROMB HAEMOST | 2015 | Pannexin-1 | Platelets | Collagen induces ATP release from blood platelets and leads to platelet aggregation [32] |
| Calder, B.W. | Yost, M.J. | TISSUE ENG | 2015 | Connexin 43 | HMVEC | CX43 mediated ATP release in HMVEC was decreased upon treatment with a CX43 mimetic peptide (JM2) and FFAs [33] |
| Csóka, B. | Haskó, G. | FASEB | 2015 | Connexin 43 | - | ATP is released during sepsis and CX43 blocking leads to increased inflammatory cytokines and bacterial load [34] |
| Ren, H. | Qian, M. | INFECT IMMUN | 2014 | Exocytosis | Macrophages | ATP is released from macrophages through TLR activation upon stimulation with LPS and Pam3CSK4 [35] |
| Taylor, K.A. | Mahaut-Smith, M.P. | J THROMB HAEMOST | 2014 | Pannexin-1 | Platelets | Arterial shear rates induce ATP release via PANX1 in vitro, which ATP interacts with P2X1 and leads to platelet aggregation [36] |
| Imura, Y. | Koizumi, S. | GLIA | 2013 | Exocytosis | Microglia | Stimulation with ionomycin or LPS induces release of ATP from microglia by increasing VNUT-dependent exocytotic mechanisms [19] |
| Sakaki, H. | Kojima, S. | PLOS ONE | 2013 | Exocytosis | THP-1 monocytes | LPS induced ATP release leads to autocrine P2Y11 activation, M1 polarization and cytokines secretion [37] |