Key result
PKCδ deficiency in mice increases white blood cells and platelets, accelerating recovery from thrombocytopenia.
Why the study?
Does Protein Kinase C δ (PKCδ) deficiency enhance megakaryopoiesis and recovery from thrombocytopenia in mice?
Population
PKCδ(-/-) and wild-type littermate mice
Comparison
Protein Kinase C δ deficiency vs Wild-type littermate mice
Design
Preclinical
Authors
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May support PKCδ as a thrombocytopenia target in mice; leaves open human translation and should not change practice.
Does Protein Kinase C δ (PKCδ) deficiency enhance megakaryopoiesis and recovery from thrombocytopenia in mice?
p-value: p=<0.05
PKCδ deficiency enhances megakaryopoiesis and accelerates recovery from thrombocytopenia, suggesting PKCδ as a potential therapeutic target for thrombocytopenia.
Kostyak et al. (2014) studied Thrombocytopenia. PKCδ deficiency vs. Wild-type littermate mice was evaluated on White blood cell and platelet counts, bone marrow and splenic megakaryocytes (p=<0.05). PKCδ deficiency in mice caused an increase in white blood cells, platelet counts, and megakaryocytes (P<0.05), and led to faster recovery from thrombocytopenic challenge compared with wild-type.
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