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Trp53 regulates platelets in bone marrow via the PI3K pathway
The p53 gene is well known as a key tumor suppressor gene; it is vital for hematopoietic stem cell differentiation and growth. In the present study, the change of platelets (PLTs) in p53 knockout mice (p53(-/-) mice) was investigated. The peripheral blood cell subsets and PLT parameters in p53(-/-)m...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388439/ https://www.ncbi.nlm.nih.gov/pubmed/32765666 http://dx.doi.org/10.3892/etm.2020.8850 |
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author | Yang, Mingming Liu, Qing Niu, Ting Kuang, Jianbiao Zhang, Xiaohan Jiang, Lingbi Li, Siqi He, Xiaodong Wang, Lijing Li, Jiangchao |
author_facet | Yang, Mingming Liu, Qing Niu, Ting Kuang, Jianbiao Zhang, Xiaohan Jiang, Lingbi Li, Siqi He, Xiaodong Wang, Lijing Li, Jiangchao |
author_sort | Yang, Mingming |
collection | PubMed |
description | The p53 gene is well known as a key tumor suppressor gene; it is vital for hematopoietic stem cell differentiation and growth. In the present study, the change of platelets (PLTs) in p53 knockout mice (p53(-/-) mice) was investigated. The peripheral blood cell subsets and PLT parameters in p53(-/-)mice were compared with those in age-matched p53(+/+) mice. Bleeding time as well as the alteration of PLT levels, were analyzed with the PLT marker CD41 antibody using flow cytometry. The results revealed that the number of PLTs in p53(-/-) mice was significantly lower than that in p53(+/+) mice. Bleeding time was prolonged in the peripheral blood of p53(-/-) mice compared with that of p53(+/+) mice. Furthermore, the related gene expression of the PI3K signaling pathway in the bone marrow of p53(-/-) mice was shown to be associated with plateletogenesis. PI3K inhibitor (LY294002) was also used to treat p53(-/-) mice, and the results demonstrated that LY294002 revert the change of PLTs in these mice. In summary, PLTs were altered in p53(-/-) mice, and the PI3K signaling pathway was involved in that process, suggesting that the p53-dependent PI3K signaling pathway is involved in thrombocytopenia or PLT diseases. PLT number is reduced in p53 deficiency; however, this reduction could be reverted by inhibiting the PI3K pathway. |
format | Online Article Text |
id | pubmed-7388439 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73884392020-08-05 Trp53 regulates platelets in bone marrow via the PI3K pathway Yang, Mingming Liu, Qing Niu, Ting Kuang, Jianbiao Zhang, Xiaohan Jiang, Lingbi Li, Siqi He, Xiaodong Wang, Lijing Li, Jiangchao Exp Ther Med Articles The p53 gene is well known as a key tumor suppressor gene; it is vital for hematopoietic stem cell differentiation and growth. In the present study, the change of platelets (PLTs) in p53 knockout mice (p53(-/-) mice) was investigated. The peripheral blood cell subsets and PLT parameters in p53(-/-)mice were compared with those in age-matched p53(+/+) mice. Bleeding time as well as the alteration of PLT levels, were analyzed with the PLT marker CD41 antibody using flow cytometry. The results revealed that the number of PLTs in p53(-/-) mice was significantly lower than that in p53(+/+) mice. Bleeding time was prolonged in the peripheral blood of p53(-/-) mice compared with that of p53(+/+) mice. Furthermore, the related gene expression of the PI3K signaling pathway in the bone marrow of p53(-/-) mice was shown to be associated with plateletogenesis. PI3K inhibitor (LY294002) was also used to treat p53(-/-) mice, and the results demonstrated that LY294002 revert the change of PLTs in these mice. In summary, PLTs were altered in p53(-/-) mice, and the PI3K signaling pathway was involved in that process, suggesting that the p53-dependent PI3K signaling pathway is involved in thrombocytopenia or PLT diseases. PLT number is reduced in p53 deficiency; however, this reduction could be reverted by inhibiting the PI3K pathway. D.A. Spandidos 2020-08 2020-06-09 /pmc/articles/PMC7388439/ /pubmed/32765666 http://dx.doi.org/10.3892/etm.2020.8850 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yang, Mingming Liu, Qing Niu, Ting Kuang, Jianbiao Zhang, Xiaohan Jiang, Lingbi Li, Siqi He, Xiaodong Wang, Lijing Li, Jiangchao Trp53 regulates platelets in bone marrow via the PI3K pathway |
title | Trp53 regulates platelets in bone marrow via the PI3K pathway |
title_full | Trp53 regulates platelets in bone marrow via the PI3K pathway |
title_fullStr | Trp53 regulates platelets in bone marrow via the PI3K pathway |
title_full_unstemmed | Trp53 regulates platelets in bone marrow via the PI3K pathway |
title_short | Trp53 regulates platelets in bone marrow via the PI3K pathway |
title_sort | trp53 regulates platelets in bone marrow via the pi3k pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388439/ https://www.ncbi.nlm.nih.gov/pubmed/32765666 http://dx.doi.org/10.3892/etm.2020.8850 |
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