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Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II
Human fibronectin receptor (VLA-5) alpha and beta chain probes were used to identify their mouse homologues in a thioglycollate-elicited peritoneal exudate cell cDNA library. Sequence analysis of both alpha and beta chain-related murine clones revealed approximately 90% homology to their human count...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1989
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189309/ https://www.ncbi.nlm.nih.gov/pubmed/2523953 |
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collection | PubMed |
description | Human fibronectin receptor (VLA-5) alpha and beta chain probes were used to identify their mouse homologues in a thioglycollate-elicited peritoneal exudate cell cDNA library. Sequence analysis of both alpha and beta chain-related murine clones revealed approximately 90% homology to their human counterparts by both nucleotide and derived amino acid sequence comparisons. Detectable alpha chain transcripts were seen predominantly in total RNA of peritoneal macrophages. beta chain expression, however, was detected at higher levels in lung, heart, brain, and kidney, suggesting the presence of a large murine VLA family similar to the human family. Analysis of levels of expression comparing resting peritoneal macrophages with macrophages elicited using inflammatory stimuli indicated that alpha chain message and surface VLA-5 expression were significantly increased using thioglycollate or Listeria monocytogenes as stimuli to elicit cells. Interestingly, beta chain message was unaffected by these inflammatory stimuli, suggesting that VLA-5 expression is regulated by VLA-5 alpha chain message levels. These results indicate that macrophage VLA-5 expression can be modulated in vivo and may provide an important mechanism by which macrophages are recruited to or adhere to fibronectin in inflammatory foci. |
format | Text |
id | pubmed-2189309 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1989 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21893092008-04-17 Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II J Exp Med Articles Human fibronectin receptor (VLA-5) alpha and beta chain probes were used to identify their mouse homologues in a thioglycollate-elicited peritoneal exudate cell cDNA library. Sequence analysis of both alpha and beta chain-related murine clones revealed approximately 90% homology to their human counterparts by both nucleotide and derived amino acid sequence comparisons. Detectable alpha chain transcripts were seen predominantly in total RNA of peritoneal macrophages. beta chain expression, however, was detected at higher levels in lung, heart, brain, and kidney, suggesting the presence of a large murine VLA family similar to the human family. Analysis of levels of expression comparing resting peritoneal macrophages with macrophages elicited using inflammatory stimuli indicated that alpha chain message and surface VLA-5 expression were significantly increased using thioglycollate or Listeria monocytogenes as stimuli to elicit cells. Interestingly, beta chain message was unaffected by these inflammatory stimuli, suggesting that VLA-5 expression is regulated by VLA-5 alpha chain message levels. These results indicate that macrophage VLA-5 expression can be modulated in vivo and may provide an important mechanism by which macrophages are recruited to or adhere to fibronectin in inflammatory foci. The Rockefeller University Press 1989-05-01 /pmc/articles/PMC2189309/ /pubmed/2523953 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title | Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title_full | Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title_fullStr | Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title_full_unstemmed | Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title_short | Molecular cloning of a murine fibronectin receptor and its expression during inflammation. Expression of VLA-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class II |
title_sort | molecular cloning of a murine fibronectin receptor and its expression during inflammation. expression of vla-5 is increased in activated peritoneal macrophages in a manner discordant from major histocompatibility complex class ii |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189309/ https://www.ncbi.nlm.nih.gov/pubmed/2523953 |