| First Author | Jansen AJ | Year | 2012 |
| Journal | Blood | Volume | 119 |
| Issue | 5 | Pages | 1263-73 |
| PubMed ID | 22101895 | Mgi Jnum | J:181795 |
| Mgi Id | MGI:5314187 | Doi | 10.1182/blood-2011-05-355628 |
| Citation | Jansen AJ, et al. (2012) Desialylation accelerates platelet clearance after refrigeration and initiates GPIbalpha metalloproteinase-mediated cleavage in mice. Blood 119(5):1263-73 |
| abstractText | When refrigerated platelets are rewarmed, they secrete active sialidases, including the lysosomal sialidase Neu1, and express surface Neu3 that remove sialic acid from platelet von Willebrand factor receptor (VWFR), specifically the GPIbalpha subunit. The recovery and circulation of refrigerated platelets is greatly improved by storage in the presence of inhibitors of sialidases. Desialylated VWFR is also a target for metalloproteinases (MPs), because GPIbalpha and GPV are cleaved from the surface of refrigerated platelets. Receptor shedding is inhibited by the MP inhibitor GM6001 and does not occur in Adam17(DeltaZn/DeltaZn) platelets expressing inactive ADAM17. Critically, desialylation in the absence of MP-mediated receptor shedding is sufficient to cause the rapid clearance of platelets from circulation. Desialylation of platelet VWFR therefore triggers platelet clearance and primes GPIbalpha and GPV for MP-dependent cleavage. |
