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Blood. 2019 Jan 24;133(4):331-343. doi: 10.1182/blood-2018-09-877787. Epub 2018 Nov 14.

The Gp1ba-Cre transgenic mouse: a new model to delineate platelet and leukocyte functions.

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Institute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
The Jackson Laboratory, Bar Harbor, ME.
Laboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, New York, NY.
Division of Rheumatology, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center and Howard Hughes Medical Institute, University of California, San Francisco, CA.
Laura and Isaac Perlmutter Cancer Center, New York University Langone Health, New York, NY; and.
Institute of Microbiology and Infection, University of Birmingham, Birmingham, United Kingdom.


Conditional knockout (KO) mouse models are invaluable for elucidating the physiological roles of platelets. The Platelet factor 4-Cre recombinase (Pf4-Cre) transgenic mouse is the current model of choice for generating megakaryocyte/platelet-specific KO mice. Platelets and leukocytes work closely together in a wide range of disease settings, yet the specific contribution of platelets to these processes remains unclear. This is partially a result of the Pf4-Cre transgene being expressed in a variety of leukocyte populations. To overcome this issue, we developed a Gp1ba-Cre transgenic mouse strain in which Cre expression is driven by the endogenous Gp1ba locus. By crossing Gp1ba-Cre and Pf4-Cre mice to the mT/mG dual-fluorescence reporter mouse and performing a head-to-head comparison, we demonstrate more stringent megakaryocyte lineage-specific expression of the Gp1ba-Cre transgene. Broader tissue expression was observed with the Pf4-Cre transgene, leading to recombination in many hematopoietic lineages, including monocytes, macrophages, granulocytes, and dendritic and B and T cells. Direct comparison of phenotypes of Csk, Shp1, or CD148 conditional KO mice generated using either the Gp1ba-Cre or Pf4-Cre strains revealed similar platelet phenotypes. However, additional inflammatory and immunological anomalies were observed in Pf4-Cre-generated KO mice as a result of nonspecific deletion in other hematopoietic lineages. By excluding leukocyte contributions to phenotypes, the Gp1ba-Cre mouse will advance our understanding of the role of platelets in inflammation and other pathophysiological processes in which platelet-leukocyte interactions are involved.

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