| First Author | Piguet PF | Year | 2001 |
| Journal | Eur J Cell Biol | Volume | 80 |
| Issue | 2 | Pages | 171-7 |
| PubMed ID | 11302522 | Mgi Jnum | J:102596 |
| Mgi Id | MGI:3607818 | Doi | 10.1078/0171-9335-00147 |
| Citation | Piguet PF, et al. (2001) Beta2 integrin modulates platelet caspase activation and life span in mice. Eur J Cell Biol 80(2):171-7 |
| abstractText | We explored the role of CD18 (beta2 integrin) in platelet physiology, using mice genetically deficient in CD18 (CD18 -/-), or its main ligand CD54 (ICAM-1, CD54 -/-). CD18 and CD11a were evident in platelets from +/+, but not from CD18 -/- mice, as seen by immunofluorescence or Western blots. CD18 mRNA was also detectable by RT-PCR in platelets from +/+, but not from CD18 -/- mice. The life span of platelets was significantly shorter in CD18 -/- than in +/+ or CD54 -/- mice, as seen by in vivo biotinylation. When a local inflammation was elicited by the intra-tracheal injection of TNF, labeled platelets from +/+, but not from CD18 -/- donors, did localize in the lung. The content of Bcl-3 was about 20-fold higher in platelet from CD18 -/-, than in those from +/+ or CD54 -/- donors, as seen on Western blots or by immunofluorescence and flow cytometry, while the amount of pro-caspase-3 was decreased. An activation of caspases in platelets from CD18 -/- was also evidenced by protease assays. Accordingly, gelsolin, a protein cleaved by caspase-3, showed a low-molecular-weight band in platelets from CD18 -/- but not from +/+ donors. These results demonstrate that the beta2 integrin, present in mouse platelets, modulates caspase activation and consequently platelet life span and response to TNF. |
