ArticleJournal of thrombosis and thrombolysis2015
Understanding thrombocytopenia: physiological role of microRNA in survival of neonatal megakaryocytes.
Article in Journal of thrombosis and thrombolysis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Epigenetic regulation of megakaryopoiesis and platelet formation.Haematologica · 2024Review
- Fetal vs adult megakaryopoiesis.Blood · 2022Article
- Changes in megakaryopoiesis over ontogeny and their implications in health and disease.Platelets · 2020Review
- Megakaryocyte ontogeny: Clinical and molecular significance.Experimental hematology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonates are predisposed to developing thrombocytopenia and neonates are affected by megakaryocytic disorders such as thrombocytopenia with absent radius syndrome and transient myeloproliferative disorder. Small double stranded non-coding microRNAs (miRNAs) have been shown to crucially involve in the regulation of stem-cell differentiation in normal as well as malignant haematopoiesis. The regulatory mechanism in developmental megakaryocytopoiesis and role of miRNAs in biological differences between adult and neonatal megakaryopoiesis is unknown. Here in we compared miR-99a levels in megakaryocytes (MKs) derived from cord blood (CB) and peripheral blood using qRT-PCR. CTDSPL is predicted as potential target of miR-99a and was confirmed by western blot. CTDSPL is shown to involve in regulation of cell growth and differentiation and exhibits tumor suppressor activity. We believe that miR-99a regulates CTDSPL, which induces the G1/S transition by increasing Cyclin expression and play a significant role in proliferation of CB-MKs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.