Research output: Contribution to journal › Article
Rights statement: © 2013 Gray et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Licence: Creative Commons: Attribution (CC-BY)
| Original language | English |
|---|---|
| Article number | 12 |
| Number of pages | 8 |
| Journal | Journal of inflammation |
| Volume | 10 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 21 Mar 2013 |
BACKGROUND: Activation of NADPH oxidase is required for neutrophil extracellular trap (NET) formation. Protein kinase C (PKC) is an upstream mediator of NADPH oxidase activation and thus likely to have a role in NET formation.
METHODS: Pharmacological inhibitors were used to block PKC activity in neutrophils harvested from healthy donor blood.
RESULTS: Pan PKC inhibition with Ro-31-8220 (p<0.001), conventional PKC inhibition with Go 6976 (p<0.001) and specific PKCβ inhibition with LY333531 (p<0.01) blocked NET formation in response to PMA. Inhibition of novel and atypical PKC had no effect. LY333531 blocked NET induction by the diacylglycerol analogue OAG (conventional PKC activator) (p<0.001).
CONCLUSIONS: Conventional PKCs have a prominent role in NET formation. Furthermore PKCβ is the major isoform implicated in NET formation.
ID: 8536980
