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Journal Article

beta 1 integrin-mediated signals are required for platelet granule secretion and hemostasis in mouse

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons118507

Petzold,  Tobias
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78591

Ruppert,  Raphael
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78485

Pandey,  Dharmendra
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78397

Meyer,  Hannelore
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78420

Moser,  Markus
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Petzold, T., Ruppert, R., Pandey, D., Barocke, V., Meyer, H., Lorenz, M., et al. (2013). beta 1 integrin-mediated signals are required for platelet granule secretion and hemostasis in mouse. BLOOD, 122(15), 2723-2731. doi:10.1182/blood-2013-06-508721.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-C2E5-6
Abstract
Integrins are critical for platelet adhesion and aggregation during arterial thrombosis and hemostasis. Although the platelet-specific aIIbb3 integrin is known to be crucial for these processes, the in vivo role of beta 1 integrins is a matter of debate. Here we demonstrate that mice expressing reduced levels of beta 1 integrins or an activationdeficient beta 1 integrin show strongly reduced platelet adhesion to collagen in vitro and in a carotis ligation model in vivo. Interestingly, hypomorphic mice expressing only 3% of beta 1 integrins on platelets show normal bleeding times despite reduced platelet adhesion. The residual 3% of beta 1 integrins are able to trigger intracellular signals driving Rac-12 dependent granule release required for platelet aggregation and hemostasis. Our findings support a model, in which platelet beta 1 integrins serve as an important signaling receptor rather than an adhesion receptor in vivo and therefore promote beta 1 integrins as a promising and so far clinically unemployed antithrombotic target.