Transcriptional Regulation of Cytosol and Membrane Alanyl-Aminopeptidase in Human TCell Subsets
Identifieur interne : 001854 ( Main/Exploration ); précédent : 001853; suivant : 001855Transcriptional Regulation of Cytosol and Membrane Alanyl-Aminopeptidase in Human TCell Subsets
Auteurs : A. Bukowska ; J. Tadje ; M. Arndt ; C. Wolke ; T. K Hne ; J. Bartsch ; J. Faust ; K. Neubert ; Y. Hashimoto ; U. LendeckelSource :
- Biological Chemistry [ 1431-6730 ] ; 2003.
English descriptors
- Teeft :
- Actinonin, Aminopeptidase, Aminopeptidase inhibitors, Aminopeptidases, Antigenic peptides, Autoimmune diseases, Biochem, Black column, Boehringer mannheim, Caap, Caap expression, Caap mrna, Caap mrna expression, Caap mrnas, Cell activation, Cell populations, Cell subsets, Chem, Cytokine, Cytosol, Ethidium bromide, Fetal calf serum, Hersh, Immunol, Inhibitor, Lendeckel, Leucine aminopeptidase, Lymphocyte, Maap, Maap expression, Maap mrna, Maap mrna levels, Maap mrnas, Major histocompatibility, Mononuclear cells, Mrna, Peptide, Phebestin, Relative amounts, Romagnani, Subset, Surface expression, Treg, Treg cells.
Abstract
Aminopeptidase inhibitors strongly affect the proliferation and function of immune cells in man and animals and are promising agents for the pharmacological treatment of inflammatory or autoimmune diseases. Membrane alanyl-aminopeptidase (mAAP) has been considered as the major target of these anti-inflammatory aminopeptidase inhibitors. Recent evidence also points to a role of the cytosol alanylaminopeptidase (cAAP) in the immune response. In this study we used quantitative RT-PCR to determine the mRNA expression of both cAAP and mAAP in resting and activated peripheral T cells and also in CD4+, CD8+, Th1, Th2 and Treg (CD4+CD25+) subpopulations. Both mAAP and cAAP mRNAs were expressed in all cell types investigated, and in response to activation their expression appeared to be upregulated in CD8+ cells, but downregulated in Treg cells. In CD4+ cells, mAAP and cAAP mRNAs were affected in opposite ways in response to activation. The cAAPspecific inhibitor, PAQ-22, did not affect either cAAP or mAAP expression in activated CD4+ or CD8+ cells, whereas in activated Treg cells it markedly upregulated the mRNA levels of both aminopeptidases. The nondiscriminatory inhibitor, phebestin, significantly increased the amount of mAAP and cAAP mRNA in CD4+ and that of cAAP in Treg cells.
Url:
DOI: 10.1515/BC.2003.073
Affiliations:
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Bukowska</name></author><author><name sortKey="Tadje, J" sort="Tadje, J" uniqKey="Tadje J" first="J." last="Tadje">J. Tadje</name></author><author><name sortKey="Arndt, M" sort="Arndt, M" uniqKey="Arndt M" first="M." last="Arndt">M. Arndt</name></author><author><name sortKey="Wolke, C" sort="Wolke, C" uniqKey="Wolke C" first="C." last="Wolke">C. Wolke</name></author><author><name sortKey="K Hne, T" sort="K Hne, T" uniqKey="K Hne T" first="T." last="K Hne">T. K Hne</name></author><author><name sortKey="Bartsch, J" sort="Bartsch, J" uniqKey="Bartsch J" first="J." last="Bartsch">J. Bartsch</name></author><author><name sortKey="Faust, J" sort="Faust, J" uniqKey="Faust J" first="J." last="Faust">J. Faust</name></author><author><name sortKey="Neubert, K" sort="Neubert, K" uniqKey="Neubert K" first="K." last="Neubert">K. Neubert</name></author><author><name sortKey="Hashimoto, Y" sort="Hashimoto, Y" uniqKey="Hashimoto Y" first="Y." last="Hashimoto">Y. Hashimoto</name></author><author><name sortKey="Lendeckel, U" sort="Lendeckel, U" uniqKey="Lendeckel U" first="U." last="Lendeckel">U. Lendeckel</name></author></analytic><monogr></monogr><series><title level="j" type="abbrev">Biological Chemistry</title><idno type="ISSN">1431-6730</idno><imprint><publisher>Walter de Gruyter</publisher><date>2003</date><date type="e-published">2005</date><biblScope unit="vol">384</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="657">657</biblScope><biblScope unit="page" to="665">665</biblScope></imprint><idno type="ISSN">1431-6730</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1431-6730</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Actinonin</term><term>Aminopeptidase</term><term>Aminopeptidase inhibitors</term><term>Aminopeptidases</term><term>Antigenic peptides</term><term>Autoimmune diseases</term><term>Biochem</term><term>Black column</term><term>Boehringer mannheim</term><term>Caap</term><term>Caap expression</term><term>Caap mrna</term><term>Caap mrna expression</term><term>Caap mrnas</term><term>Cell activation</term><term>Cell populations</term><term>Cell subsets</term><term>Chem</term><term>Cytokine</term><term>Cytosol</term><term>Ethidium bromide</term><term>Fetal calf serum</term><term>Hersh</term><term>Immunol</term><term>Inhibitor</term><term>Lendeckel</term><term>Leucine aminopeptidase</term><term>Lymphocyte</term><term>Maap</term><term>Maap expression</term><term>Maap mrna</term><term>Maap mrna levels</term><term>Maap mrnas</term><term>Major histocompatibility</term><term>Mononuclear cells</term><term>Mrna</term><term>Peptide</term><term>Phebestin</term><term>Relative amounts</term><term>Romagnani</term><term>Subset</term><term>Surface expression</term><term>Treg</term><term>Treg cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aminopeptidase inhibitors strongly affect the proliferation and function of immune cells in man and animals and are promising agents for the pharmacological treatment of inflammatory or autoimmune diseases. Membrane alanyl-aminopeptidase (mAAP) has been considered as the major target of these anti-inflammatory aminopeptidase inhibitors. Recent evidence also points to a role of the cytosol alanylaminopeptidase (cAAP) in the immune response. In this study we used quantitative RT-PCR to determine the mRNA expression of both cAAP and mAAP in resting and activated peripheral T cells and also in CD4+, CD8+, Th1, Th2 and Treg (CD4+CD25+) subpopulations. Both mAAP and cAAP mRNAs were expressed in all cell types investigated, and in response to activation their expression appeared to be upregulated in CD8+ cells, but downregulated in Treg cells. In CD4+ cells, mAAP and cAAP mRNAs were affected in opposite ways in response to activation. The cAAPspecific inhibitor, PAQ-22, did not affect either cAAP or mAAP expression in activated CD4+ or CD8+ cells, whereas in activated Treg cells it markedly upregulated the mRNA levels of both aminopeptidases. The nondiscriminatory inhibitor, phebestin, significantly increased the amount of mAAP and cAAP mRNA in CD4+ and that of cAAP in Treg cells.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Arndt, M" sort="Arndt, M" uniqKey="Arndt M" first="M." last="Arndt">M. Arndt</name><name sortKey="Bartsch, J" sort="Bartsch, J" uniqKey="Bartsch J" first="J." last="Bartsch">J. Bartsch</name><name sortKey="Bukowska, A" sort="Bukowska, A" uniqKey="Bukowska A" first="A." last="Bukowska">A. Bukowska</name><name sortKey="Faust, J" sort="Faust, J" uniqKey="Faust J" first="J." last="Faust">J. Faust</name><name sortKey="Hashimoto, Y" sort="Hashimoto, Y" uniqKey="Hashimoto Y" first="Y." last="Hashimoto">Y. Hashimoto</name><name sortKey="K Hne, T" sort="K Hne, T" uniqKey="K Hne T" first="T." last="K Hne">T. K Hne</name><name sortKey="Lendeckel, U" sort="Lendeckel, U" uniqKey="Lendeckel U" first="U." last="Lendeckel">U. Lendeckel</name><name sortKey="Neubert, K" sort="Neubert, K" uniqKey="Neubert K" first="K." last="Neubert">K. Neubert</name><name sortKey="Tadje, J" sort="Tadje, J" uniqKey="Tadje J" first="J." last="Tadje">J. Tadje</name><name sortKey="Wolke, C" sort="Wolke, C" uniqKey="Wolke C" first="C." last="Wolke">C. Wolke</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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