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Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK

The CMK cell line is an acute megakaryoblastic leukemia cell line established from a patient with Down's syndrome, and is known to possess characteristics of normal megakaryocytes. Several cytokines with the ability to stimulate megakaryopoiesis, such as interleukin‐3 (IL‐3), interleukin‐6 (IL‐...

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Detalles Bibliográficos
Autores principales: Akiyama, Yasuto, Yamaguchi, Ken, Sato, Takeyuki, Abe, Kaoru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918975/
https://www.ncbi.nlm.nih.gov/pubmed/1429211
http://dx.doi.org/10.1111/j.1349-7006.1992.tb02012.x
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author Akiyama, Yasuto
Yamaguchi, Ken
Sato, Takeyuki
Abe, Kaoru
author_facet Akiyama, Yasuto
Yamaguchi, Ken
Sato, Takeyuki
Abe, Kaoru
author_sort Akiyama, Yasuto
collection PubMed
description The CMK cell line is an acute megakaryoblastic leukemia cell line established from a patient with Down's syndrome, and is known to possess characteristics of normal megakaryocytes. Several cytokines with the ability to stimulate megakaryopoiesis, such as interleukin‐3 (IL‐3), interleukin‐6 (IL‐6) and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), stimulated colony formation by CMK cells. The present study revealed that tumor necrosis factor‐α (TNF‐α) stimulated colony formation by CMK cells; the potency was almost equal to that of IL‐3, IL‐6 or GM‐CSF. Scatchard plot analysis revealed that CMK cells possess two types of specific binding sites for TNF‐α. The high‐affinity binding sites had an affinity constant of 0.18 nM, and numbered 5,000. The low‐affinity binding sites had an affinity constant of 1.8 nM/and numbered 19,000. These results raise the possibility that TNF‐α can act as a growth‐stimulating agent on megakaryocyte‐Iineage cell line.
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spelling pubmed-59189752018-05-11 Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK Akiyama, Yasuto Yamaguchi, Ken Sato, Takeyuki Abe, Kaoru Jpn J Cancer Res Article The CMK cell line is an acute megakaryoblastic leukemia cell line established from a patient with Down's syndrome, and is known to possess characteristics of normal megakaryocytes. Several cytokines with the ability to stimulate megakaryopoiesis, such as interleukin‐3 (IL‐3), interleukin‐6 (IL‐6) and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), stimulated colony formation by CMK cells. The present study revealed that tumor necrosis factor‐α (TNF‐α) stimulated colony formation by CMK cells; the potency was almost equal to that of IL‐3, IL‐6 or GM‐CSF. Scatchard plot analysis revealed that CMK cells possess two types of specific binding sites for TNF‐α. The high‐affinity binding sites had an affinity constant of 0.18 nM, and numbered 5,000. The low‐affinity binding sites had an affinity constant of 1.8 nM/and numbered 19,000. These results raise the possibility that TNF‐α can act as a growth‐stimulating agent on megakaryocyte‐Iineage cell line. Blackwell Publishing Ltd 1992-09 /pmc/articles/PMC5918975/ /pubmed/1429211 http://dx.doi.org/10.1111/j.1349-7006.1992.tb02012.x Text en
spellingShingle Article
Akiyama, Yasuto
Yamaguchi, Ken
Sato, Takeyuki
Abe, Kaoru
Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title_full Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title_fullStr Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title_full_unstemmed Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title_short Tumor Necrosis Factor‐a Stimulates Colony Formation by a Megakaryoblastic Leukemia Cell Line, CMK
title_sort tumor necrosis factor‐a stimulates colony formation by a megakaryoblastic leukemia cell line, cmk
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918975/
https://www.ncbi.nlm.nih.gov/pubmed/1429211
http://dx.doi.org/10.1111/j.1349-7006.1992.tb02012.x
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