Published online Nov 6, 2016. doi: 10.5315/wjh.v5.i4.88
Peer-review started: July 21, 2016
First decision: August 5, 2016
Revised: August 31, 2016
Accepted: September 21, 2016
Article in press: September 23, 2016
Published online: November 6, 2016
To determine if activation of the ATP-gated P2X7 receptor channel induces phosphatidylserine (PS) exposure in erythrocytes from multiple dog breeds.
Peripheral blood was collected from 25 dogs representing 13 pedigrees and seven crossbreeds. ATP-induced PS exposure on canine erythrocytes in vitro was assessed using a flow cytometric Annexin V binding assay.
ATP induced PS exposure in erythrocytes from all dogs studied. ATP caused PS exposure in a concentration-dependent manner with an EC50 value of 395 μmol/L. The non-P2X7 agonists, ADP or AMP, did not cause PS exposure. The P2X7 antagonist, AZ10606120, but not the P2X1 antagonist, NF449, blocked ATP-induced PS exposure.
The results indicate that ATP induces PS exposure in erythrocytes from various dog breeds and that this process is mediated by P2X7 activation.
Core tip: Phosphatidylserine (PS) exposure in erythrocytes has potential roles in erythrocyte clearance and thrombus formation. Activation of the ATP-gated P2X7 receptor channel induces PS exposure in human erythrocytes, but whether this process occurs in erythrocytes from other mammals remained hitherto unknown. The current study shows that extracellular ATP causes PS exposure in dog erythrocytes from 13 pedigrees and seven crossbreeds. Notably, the current study shows that this process is mediated by P2X7 activation. These results suggest that P2X7-mediated PS exposure on erythrocytes may have important roles in red blood cell biology in dogs.