ArticleArteriosclerosis, thrombosis, and vascular biology2014
Protein kinase C δ deficiency enhances megakaryopoiesis and recovery from thrombocytopenia.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Regulating mitochondrial oxidative phosphorylation and MAPK signaling: wedelolactone as a novel therapeutic for radiation-induced thrombocytopenia.Frontiers in pharmacology · 2025Article
- Characterization of Integrin αIIbβ3-Mediated Outside-in Signaling by Protein Kinase Cδ in Platelets.International journal of molecular sciences · 2020Article
- Role of Protein Kinase C-delta in regulating platelet activation and platelet-leukocyte interaction during sepsis.PloS one · 2018Article
- Lung injury during LPS-induced inflammation occurs independently of the receptor P2YPurinergic signalling · 2017Article
- PKC-epsilon deficiency alters progenitor cell populations in favor of megakaryopoiesis.PloS one · 2017Article
- Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Human thrombopoiesis depends on Protein kinase Cδ/protein kinase Cε functional couple.Haematologica · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe previously determined that protein kinase C δ (PKCδ) regulates platelet function. However, the function of PKCδ in megakaryopoiesis is unknown. APPROACH AND
resultsUsing PKCδ(-/-) and wild-type littermate mice, we found that deficiency of PKCδ caused an increase in white blood cells and platelet counts, as well as in bone marrow and splenic megakaryocytes (P<0.05). Additionally, the megakaryocyte number and DNA content were enhanced in PKCδ(-/-) mouse bone marrow after culturing with exogenous thrombopoietin compared with wild-type (P<0.05). Importantly, thrombopoietin-induced signaling was also altered with PKCδ deletion because both extracellular signal-regulated kinase and Akt308 phosphorylation were heightened in PKCδ(-/-) megakaryocytes compared with wild-type. Finally, PKCδ(-/-) mice recovered faster and had a heightened rebound thrombocytosis after thrombocytopenic challenge.
conclusionsThese data suggest that PKCδ is an important megakaryopoietic protein, which regulates signaling induced by thrombopoietin and represents a potential therapeutic target.
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Registered trials
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