例如:"lncRNA", "apoptosis", "WRKY"

The PI 3-kinase PI3KC2α regulates mouse platelet membrane structure and function independently of membrane lipid composition.

FEBS Lett.2019 Jan;593(1):88-96. doi:10.1002/1873-3468.13295. Epub 2018 Nov 24
Maria V Selvadurai 1 , Rose J Brazilek 1 , Mitchell J Moon 1 , Jean-Yves Rinckel 2 , Anita Eckly 2 , Christian Gachet 2 , Peter J Meikle 3 , Harshal H Nandurkar 1 , Warwick S Nesbitt 4 , Justin R Hamilton 1
Maria V Selvadurai 1 , Rose J Brazilek 1 , Mitchell J Moon 1 , Jean-Yves Rinckel 2 , Anita Eckly 2 , Christian Gachet 2 , Peter J Meikle 3 , Harshal H Nandurkar 1 , Warwick S Nesbitt 4 , Justin R Hamilton 1
+ et al

[No authors listed]

Author information
  • 1 Australian Centre for Blood Diseases, Monash University, Melbourne, Australia.
  • 2 INSERM, EFS GEST, BPPS UMR_S1225, FMTS, Université de Strasbourg, France.
  • 3 Metabolomics Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
  • 4 Microplatforms Research Group, School of Engineering, RMIT University, Melbourne, Australia.

摘要


PI3KC2α is a phosphoinositide 3-kinase with a recently reported function in platelets; PI3KC2α-deficient mouse platelets have altered membrane structure and impaired function. Yet, how these membrane changes cause platelet dysfunction remains unknown. Here, focused ion beam-scanning electron microscopy of PI3KC2α-deficient platelet ultrastructure reveals a specific effect on the internal membrane structure, while liquid chromatography-tandem mass spectrometry profiling of 294 lipid species shows unaltered lipid composition. Functionally, PI3KC2α-deficient platelets exhibit impaired thrombosis specifically under conditions involving membrane tethering. These studies indicate that the structural changes in PI3KC2α-deficient platelets are limited to the membrane, occur without major changes in lipid composition, and selectively impair cell function during thrombus formation. These findings illustrate a unique mechanism that may be targetable for anti-thrombotic benefit.

KEYWORDS: open canalicular system, phosphoinositide 3-kinase, platelets, thrombosis