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Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines

Apoptosis inhibitor of macrophage (AIM) is initially reported to protect macrophages from apoptosis. In this study, we determined the effect of AIM on the macrophage-derived tumor, histiocytic sarcoma cell lines (HS) of dogs. Five HS and five other tumor cell lines were used. When recombinant canine...

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Autores principales: UCHIDA, Mona, SAEKI, Kohei, MAEDA, Shingo, TAMAHARA, Satoshi, YONEZAWA, Tomohiro, MATSUKI, Naoaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Society of Veterinary Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5059382/
https://www.ncbi.nlm.nih.gov/pubmed/27246397
http://dx.doi.org/10.1292/jvms.16-0120
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author UCHIDA, Mona
SAEKI, Kohei
MAEDA, Shingo
TAMAHARA, Satoshi
YONEZAWA, Tomohiro
MATSUKI, Naoaki
author_facet UCHIDA, Mona
SAEKI, Kohei
MAEDA, Shingo
TAMAHARA, Satoshi
YONEZAWA, Tomohiro
MATSUKI, Naoaki
author_sort UCHIDA, Mona
collection PubMed
description Apoptosis inhibitor of macrophage (AIM) is initially reported to protect macrophages from apoptosis. In this study, we determined the effect of AIM on the macrophage-derived tumor, histiocytic sarcoma cell lines (HS) of dogs. Five HS and five other tumor cell lines were used. When recombinant canine AIM was applied to non-serum culture media, cell numbers of all the HS and two of other tumor cell lines decreased dose-dependently. The DNA fragmentation, TUNEL staining and flow cytometry tests revealed that AIM induced both of apoptosis and cell cycle arrest in the HS. Although AIM is known as an apoptosis inhibitor, these results suggest that a high dose of AIM could have an opposite function in HS and some tumor cell lines.
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spelling pubmed-50593822016-10-12 Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines UCHIDA, Mona SAEKI, Kohei MAEDA, Shingo TAMAHARA, Satoshi YONEZAWA, Tomohiro MATSUKI, Naoaki J Vet Med Sci Internal Medicine Apoptosis inhibitor of macrophage (AIM) is initially reported to protect macrophages from apoptosis. In this study, we determined the effect of AIM on the macrophage-derived tumor, histiocytic sarcoma cell lines (HS) of dogs. Five HS and five other tumor cell lines were used. When recombinant canine AIM was applied to non-serum culture media, cell numbers of all the HS and two of other tumor cell lines decreased dose-dependently. The DNA fragmentation, TUNEL staining and flow cytometry tests revealed that AIM induced both of apoptosis and cell cycle arrest in the HS. Although AIM is known as an apoptosis inhibitor, these results suggest that a high dose of AIM could have an opposite function in HS and some tumor cell lines. The Japanese Society of Veterinary Science 2016-05-30 2016-09 /pmc/articles/PMC5059382/ /pubmed/27246397 http://dx.doi.org/10.1292/jvms.16-0120 Text en ©2016 The Japanese Society of Veterinary Science http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.
spellingShingle Internal Medicine
UCHIDA, Mona
SAEKI, Kohei
MAEDA, Shingo
TAMAHARA, Satoshi
YONEZAWA, Tomohiro
MATSUKI, Naoaki
Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title_full Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title_fullStr Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title_full_unstemmed Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title_short Apoptosis inhibitor of macrophage (AIM) reduces cell number in canine histiocytic sarcoma cell lines
title_sort apoptosis inhibitor of macrophage (aim) reduces cell number in canine histiocytic sarcoma cell lines
topic Internal Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5059382/
https://www.ncbi.nlm.nih.gov/pubmed/27246397
http://dx.doi.org/10.1292/jvms.16-0120
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