Prat, Christine M. A.; Schmid, Sonja; Farrugia, Fanny; Cenac, Nicolas; Masson, Gwendal Le; Schwemmle, Martin; Gonzalez-Dunia, Daniel Mutation of the Protein Kinase C Site in Borna Disease Virus Phosphoprotein Abrogates Viral Interference with Neuronal Signaling and Restores Normal Synaptic Activity Journal Article In: PLoS Pathog, vol. 5, no. 5, 2009, ISSN: 1553-7374. @article{Prat2009,
title = {Mutation of the Protein Kinase C Site in Borna Disease Virus Phosphoprotein Abrogates Viral Interference with Neuronal Signaling and Restores Normal Synaptic Activity},
author = {Christine M. A. Prat and Sonja Schmid and Fanny Farrugia and Nicolas Cenac and Gwendal Le Masson and Martin Schwemmle and Daniel Gonzalez-Dunia},
editor = {Raul Andino},
doi = {10.1371/journal.ppat.1000425},
issn = {1553-7374},
year = {2009},
date = {2009-05-08},
urldate = {2009-05-08},
journal = {PLoS Pathog},
volume = {5},
number = {5},
publisher = {Public Library of Science (PLoS)},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Dejean, A. S.; Beisner, D. R.; Ch'en, I. L.; Kerdiles, Y. M.; Babour, A.; Arden, K. C.; Castrillon, D. H.; DePinho, R. A.; Hedrick, S. M. Transcription factor Foxo3 controls the magnitude of T cell immune responses by modulating the function of dendritic cells Journal Article In: Nat Immunol, vol. 10, no. 5, pp. 504-13, 2009, ISSN: 1529-2916 (Electronic)
1529-2908 (Linking). @article{RN19,
title = {Transcription factor Foxo3 controls the magnitude of T cell immune responses by modulating the function of dendritic cells},
author = {Dejean, A. S. and Beisner, D. R. and Ch'en, I. L. and Kerdiles, Y. M. and Babour, A. and Arden, K. C. and Castrillon, D. H. and DePinho, R. A. and Hedrick, S. M.},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19363483},
doi = {10.1038/ni.1729},
issn = {1529-2916 (Electronic)
1529-2908 (Linking)},
year = {2009},
date = {2009-01-01},
journal = {Nat Immunol},
volume = {10},
number = {5},
pages = {504-13},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Karim, Zoubida; Gérard, Bénédicte; Bakouh, Naziha; Alili, Rohia; Leroy, Christine; Beck, Laurent; Silve, Caroline; Planelles, Gabrielle; Urena-Torres, Pablo; Grandchamp, Bernard; Friedlander, Gérard; Prié, Dominique NHERF1 mutations and responsiveness of renal parathyroid hormone Journal Article In: The New England Journal of Medicine, vol. 359, no. 11, pp. 1128–1135, 2008, ISSN: 1533-4406. @article{karim_nherf1_2008,
title = {NHERF1 mutations and responsiveness of renal parathyroid hormone},
author = {Karim, Zoubida and Gérard, Bénédicte and Bakouh, Naziha and Alili, Rohia and Leroy, Christine and Beck, Laurent and Silve, Caroline and Planelles, Gabrielle and Urena-Torres, Pablo and Grandchamp, Bernard and Friedlander, Gérard and Prié, Dominique},
doi = {10.1056/NEJMoa0802836},
issn = {1533-4406},
year = {2008},
date = {2008-09-01},
journal = {The New England Journal of Medicine},
volume = {359},
number = {11},
pages = {1128--1135},
abstract = {Impaired renal phosphate reabsorption, as measured by dividing the tubular maximal reabsorption of phosphate by the glomerular filtration rate (TmP/GFR), increases the risks of nephrolithiasis and bone demineralization. Data from animal models suggest that sodium-hydrogen exchanger regulatory factor 1 (NHERF1) controls renal phosphate transport. We sequenced the NHERF1 gene in 158 patients, 94 of whom had either nephrolithiasis or bone demineralization. We identified three distinct mutations in seven patients with a low TmP/GFR value. No patients with normal TmP/GFR values had mutations. The mutants expressed in cultured renal cells increased the generation of cyclic AMP (cAMP) by parathyroid hormone (PTH) and inhibited phosphate transport. These NHERF1 mutations suggest a previously unrecognized cause of renal phosphate loss in humans.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Impaired renal phosphate reabsorption, as measured by dividing the tubular maximal reabsorption of phosphate by the glomerular filtration rate (TmP/GFR), increases the risks of nephrolithiasis and bone demineralization. Data from animal models suggest that sodium-hydrogen exchanger regulatory factor 1 (NHERF1) controls renal phosphate transport. We sequenced the NHERF1 gene in 158 patients, 94 of whom had either nephrolithiasis or bone demineralization. We identified three distinct mutations in seven patients with a low TmP/GFR value. No patients with normal TmP/GFR values had mutations. The mutants expressed in cultured renal cells increased the generation of cyclic AMP (cAMP) by parathyroid hormone (PTH) and inhibited phosphate transport. These NHERF1 mutations suggest a previously unrecognized cause of renal phosphate loss in humans. |
Blanchard, N.; Gonzalez, F.; Schaeffer, M.; Joncker, N. T.; Cheng, T.; Shastri, A. J.; Robey, E. A.; Shastri, N. Immunodominant, protective response to the parasite Toxoplasma gondii requires antigen processing in the endoplasmic reticulum Journal Article In: Nat Immunol, vol. 9, no. 8, pp. 937-44, 2008, (NLM
In-Process
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't DEP - 20080629). @article{b,
title = {Immunodominant, protective response to the parasite Toxoplasma gondii requires antigen processing in the endoplasmic reticulum},
author = {Blanchard, N. and Gonzalez, F. and Schaeffer, M. and Joncker, N. T. and Cheng, T. and Shastri, A. J. and Robey, E. A. and Shastri, N.},
year = {2008},
date = {2008-01-01},
journal = {Nat Immunol},
volume = {9},
number = {8},
pages = {937-44},
abstract = {The parasite Toxoplasma gondii replicates in a specialized intracellular vacuole and causes disease in many species. Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T. gondii antigens and host genes required for eliciting protective immunity are poorly defined. Here we identified GRA6, a polymorphic protein secreted in the parasitophorous vacuole, as the source of the immunodominant and protective decapeptide HF10 presented by the H-2L(d) major histocompatibility complex class I molecule. Presentation of the HF10-H-2L(d) ligand required proteolysis by ERAAP, the endoplasmic reticulum aminopeptidase associated with antigen processing. Consequently, expansion of protective CD8(+) T cell populations was impaired in T. gondii-infected ERAAP-deficient mice, which were more susceptible to toxoplasmosis. Thus, endoplasmic reticulum proteolysis is critical for eliciting protective immunity to a vacuolar parasite.},
note = {NLM
In-Process
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't DEP - 20080629},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The parasite Toxoplasma gondii replicates in a specialized intracellular vacuole and causes disease in many species. Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T. gondii antigens and host genes required for eliciting protective immunity are poorly defined. Here we identified GRA6, a polymorphic protein secreted in the parasitophorous vacuole, as the source of the immunodominant and protective decapeptide HF10 presented by the H-2L(d) major histocompatibility complex class I molecule. Presentation of the HF10-H-2L(d) ligand required proteolysis by ERAAP, the endoplasmic reticulum aminopeptidase associated with antigen processing. Consequently, expansion of protective CD8(+) T cell populations was impaired in T. gondii-infected ERAAP-deficient mice, which were more susceptible to toxoplasmosis. Thus, endoplasmic reticulum proteolysis is critical for eliciting protective immunity to a vacuolar parasite. |
Joffre, O.; Santolaria, T.; Calise, D.; Al Saati, T.; Hudrisier, D.; Romagnoli, P.; van Meerwijk, J. P. M. Prevention of acute and chronic allograft rejection with CD4+CD25+Foxp3+ regulatory T lymphocytes Journal Article In: Nature Medicine, vol. 14, no. 1, pp. 88-92, 2008. @article{RN137,
title = {Prevention of acute and chronic allograft rejection with CD4+CD25+Foxp3+ regulatory T lymphocytes},
author = {Joffre, O. and Santolaria, T. and Calise, D. and Al Saati, T. and Hudrisier, D. and Romagnoli, P. and van Meerwijk, J. P. M.},
year = {2008},
date = {2008-01-01},
journal = {Nature Medicine},
volume = {14},
number = {1},
pages = {88-92},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Joffre, O.; Santolaria, T.; van Meerwijk, J. P. M. [Tregs-based immunotherapy: an efficient way to fully inhibit acute and chronic rejection.] Journal Article In: Med Sci (Paris), vol. 24, no. 8-9, pp. 689-691, 2008, ISSN: 0767-0974 (Print). @article{RN153,
title = {[Tregs-based immunotherapy: an efficient way to fully inhibit acute and chronic rejection.]},
author = {Joffre, O. and Santolaria, T. and van Meerwijk, J.P.M.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18789210},
doi = {00/00/0C/B6/ [pii]},
issn = {0767-0974 (Print)},
year = {2008},
date = {2008-01-01},
journal = {Med Sci (Paris)},
volume = {24},
number = {8-9},
pages = {689-691},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Pomie, C.; Menager-Marcq, I.; van Meerwijk, J. P. M. Murine CD8(+) regulatory T lymphocytes: The new era Journal Article In: Hum Immunol, vol. 69, pp. 708-714, 2008, ISSN: 0198-8859 (Print). @article{RN155,
title = {Murine CD8(+) regulatory T lymphocytes: The new era},
author = {Pomie, C. and Menager-Marcq, I. and van Meerwijk, J.P.M.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18817827},
doi = {S0198-8859(08)00450-3 [pii]
10.1016/j.humimm.2008.08.288},
issn = {0198-8859 (Print)},
year = {2008},
date = {2008-01-01},
journal = {Hum Immunol},
volume = {69},
pages = {708-714},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Romagnoli, P.; Ribot, J.; Tellier, J.; van Meerwijk, J. P. M. Thymic and peripheral generation of CD4+Foxp3+ regulatory T cells Book Chapter In: Jiang, S. (Ed.): Regulatory T cells and clinical application, vol. in press, Springer, 2008, ISBN: 978-0-387-77908-9. @inbook{RN134,
title = {Thymic and peripheral generation of CD4+Foxp3+ regulatory T cells},
author = {Romagnoli, P. and Ribot, J. and Tellier, J. and van Meerwijk, J. P. M.},
editor = {Jiang, S.},
url = {http://www.springer.com/biomed/immunology/book/978-0-387-77908-9},
isbn = {978-0-387-77908-9},
year = {2008},
date = {2008-01-01},
booktitle = {Regulatory T cells and clinical application},
volume = {in press},
publisher = {Springer},
keywords = {},
pubstate = {published},
tppubtype = {inbook}
}
|
Blanchard, N.; Gonzalez, F.; Schaeffer, M.; Joncker, N. T.; Cheng, T.; Shastri, A. J.; Robey, E. A.; Shastri, N. Immunodominant, protective response to the parasite Toxoplasma gondii requires antigen processing in the endoplasmic reticulum Journal Article In: Nat Immunol, vol. 9, no. 8, pp. 937-44, 2008, (NLM
In-Process
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't DEP - 20080629). @article{b,
title = {Immunodominant, protective response to the parasite Toxoplasma gondii requires antigen processing in the endoplasmic reticulum},
author = {Blanchard, N. and Gonzalez, F. and Schaeffer, M. and Joncker, N. T. and Cheng, T. and Shastri, A. J. and Robey, E. A. and Shastri, N.},
year = {2008},
date = {2008-01-01},
journal = {Nat Immunol},
volume = {9},
number = {8},
pages = {937-44},
abstract = {The parasite Toxoplasma gondii replicates in a specialized intracellular vacuole and causes disease in many species. Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T. gondii antigens and host genes required for eliciting protective immunity are poorly defined. Here we identified GRA6, a polymorphic protein secreted in the parasitophorous vacuole, as the source of the immunodominant and protective decapeptide HF10 presented by the H-2L(d) major histocompatibility complex class I molecule. Presentation of the HF10-H-2L(d) ligand required proteolysis by ERAAP, the endoplasmic reticulum aminopeptidase associated with antigen processing. Consequently, expansion of protective CD8(+) T cell populations was impaired in T. gondii-infected ERAAP-deficient mice, which were more susceptible to toxoplasmosis. Thus, endoplasmic reticulum proteolysis is critical for eliciting protective immunity to a vacuolar parasite.},
note = {NLM
In-Process
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't DEP - 20080629},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The parasite Toxoplasma gondii replicates in a specialized intracellular vacuole and causes disease in many species. Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T. gondii antigens and host genes required for eliciting protective immunity are poorly defined. Here we identified GRA6, a polymorphic protein secreted in the parasitophorous vacuole, as the source of the immunodominant and protective decapeptide HF10 presented by the H-2L(d) major histocompatibility complex class I molecule. Presentation of the HF10-H-2L(d) ligand required proteolysis by ERAAP, the endoplasmic reticulum aminopeptidase associated with antigen processing. Consequently, expansion of protective CD8(+) T cell populations was impaired in T. gondii-infected ERAAP-deficient mice, which were more susceptible to toxoplasmosis. Thus, endoplasmic reticulum proteolysis is critical for eliciting protective immunity to a vacuolar parasite. |
Ribot, J.; Enault, G.; Pilipenko, S.; Huchencq, A.; Calise, M.; Hudrisier, D.; Romagnoli, P.; van Meerwijk, J. P. M. Shaping of the autoreactive regulatory T cell repertoire by thymic cortical positive selection Journal Article In: J. Immunol., vol. 179, pp. 6741-6748, 2007. @article{RN135,
title = {Shaping of the autoreactive regulatory T cell repertoire by thymic cortical positive selection},
author = {Ribot, J. and Enault, G. and Pilipenko, S. and Huchencq, A. and Calise, M. and Hudrisier, D. and Romagnoli, P. and van Meerwijk, J. P. M.},
year = {2007},
date = {2007-01-01},
journal = {J. Immunol.},
volume = {179},
pages = {6741-6748},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Joffre, O.; van Meerwijk, J. P. M. CD4+CD25+ regulatory T lymphocytes in bone marrow transplantation Journal Article In: Seminars in Immunology, vol. 18, no. 2, pp. 128-135, 2006. @article{RN127,
title = {CD4+CD25+ regulatory T lymphocytes in bone marrow transplantation},
author = {Joffre, O. and van Meerwijk, J. P. M.},
year = {2006},
date = {2006-01-01},
journal = {Seminars in Immunology},
volume = {18},
number = {2},
pages = {128-135},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Menager-Marcq, I.; Pomie, C.; Romagnoli, P.; van Meerwijk, J. P. M. CD8+CD28- regulatory T lymphocytes prevent experimental inflammatory bowel disease in mice Journal Article In: Gastroenterology, vol. 131, no. 6, pp. 1775-85, 2006. @article{RN132,
title = {CD8+CD28- regulatory T lymphocytes prevent experimental inflammatory bowel disease in mice},
author = {Menager-Marcq, I. and Pomie, C. and Romagnoli, P. and van Meerwijk, J. P. M.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17087950},
year = {2006},
date = {2006-01-01},
journal = {Gastroenterology},
volume = {131},
number = {6},
pages = {1775-85},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Ribot, J.; Romagnoli, P.; van Meerwijk, J. P. M. Agonist ligands expressed by thymic epithelium enhance positive selection of regulatory T lymphocytes from precursors with a normally diverse TCR-repertoire Journal Article In: J. Immunol., vol. 177, no. 2, pp. 1101-1107, 2006. @article{RN128,
title = {Agonist ligands expressed by thymic epithelium enhance positive selection of regulatory T lymphocytes from precursors with a normally diverse TCR-repertoire},
author = {Ribot, J. and Romagnoli, P. and van Meerwijk, J. P. M.},
year = {2006},
date = {2006-01-01},
journal = {J. Immunol.},
volume = {177},
number = {2},
pages = {1101-1107},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Tellier, J.; van Meerwijk, J. P. M.; Romagnoli, P. An MHC-linked locus modulates thymic differentiation of CD4+CD25+Foxp3+ regulatory T lymphocytes Journal Article In: Int Immunol, vol. 18, no. 11, pp. 1509-1519, 2006. @article{RN133,
title = {An MHC-linked locus modulates thymic differentiation of CD4+CD25+Foxp3+ regulatory T lymphocytes},
author = {Tellier, J. and van Meerwijk, J. P. M. and Romagnoli, P.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16943258},
year = {2006},
date = {2006-01-01},
journal = {Int Immunol},
volume = {18},
number = {11},
pages = {1509-1519},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Gallazzini, Morgan; Karim, Zoubida; Bichara, Maurice Regulation of ROMK (Kir 1.1) channel expression in kidney thick ascending limb by hypertonicity: role of TonEBP and MAPK pathways Journal Article In: Nephron. Physiology, vol. 104, no. 4, pp. 126–135, 2006, ISSN: 1660-2137. @article{gallazzini_regulation_2006,
title = {Regulation of ROMK (Kir 1.1) channel expression in kidney thick ascending limb by hypertonicity: role of TonEBP and MAPK pathways},
author = {Gallazzini, Morgan and Karim, Zoubida and Bichara, Maurice},
doi = {10.1159/000095855},
issn = {1660-2137},
year = {2006},
date = {2006-01-01},
journal = {Nephron. Physiology},
volume = {104},
number = {4},
pages = {126--135},
abstract = {The present study assessed the mechanisms by which hypertonicity caused by NaCl enhances the renal outer medullary potassium channel (ROMK) mRNA abundance in rat kidney medullary thick ascending limb (MTAL) and in cultured mouse TAL cells. Using the run-off technique, we observed that the ROMK gene transcription rate in nuclei isolated from MTAL fragments was enhanced approximately 40% by a high NaCl medium. In MTAL fragments, hypertonicity (450 mosm) caused by NaCl, not by mannitol or urea, enhanced both ROMK mRNA abundance and tonicity-responsive enhancer binding protein (TonEBP) total abundance and nuclear localization. In an immortalized mouse TAL cell culture in which ROMK is apically expressed, hypertonicity caused by both NaCl and mannitol, not urea, enhanced both ROMK mRNA abundance and TonEBP total abundance and nuclear localization. Confocal microscopy confirmed an increased nuclear translocation of TonEBP in response to NaCl-induced hypertonicity. Finally, inhibition of the p38 MAPK pathway by SB203580 and of the ERK pathway by PD98059 abolished the NaCl-induced stimulation of TonEBP and ROMK. These results establish that mRNA expression of ROMK is augmented in the MTAL by NaCl-induced hypertonicity through stimulation of ROMK gene transcription, and that TonEBP and the p38 MAPK and ERK pathways are involved in this effect.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The present study assessed the mechanisms by which hypertonicity caused by NaCl enhances the renal outer medullary potassium channel (ROMK) mRNA abundance in rat kidney medullary thick ascending limb (MTAL) and in cultured mouse TAL cells. Using the run-off technique, we observed that the ROMK gene transcription rate in nuclei isolated from MTAL fragments was enhanced approximately 40% by a high NaCl medium. In MTAL fragments, hypertonicity (450 mosm) caused by NaCl, not by mannitol or urea, enhanced both ROMK mRNA abundance and tonicity-responsive enhancer binding protein (TonEBP) total abundance and nuclear localization. In an immortalized mouse TAL cell culture in which ROMK is apically expressed, hypertonicity caused by both NaCl and mannitol, not urea, enhanced both ROMK mRNA abundance and TonEBP total abundance and nuclear localization. Confocal microscopy confirmed an increased nuclear translocation of TonEBP in response to NaCl-induced hypertonicity. Finally, inhibition of the p38 MAPK pathway by SB203580 and of the ERK pathway by PD98059 abolished the NaCl-induced stimulation of TonEBP and ROMK. These results establish that mRNA expression of ROMK is augmented in the MTAL by NaCl-induced hypertonicity through stimulation of ROMK gene transcription, and that TonEBP and the p38 MAPK and ERK pathways are involved in this effect. |
Bichara, Maurice; Attmane-Elakeb, Amel; Brown, Dennis; Essig, Marie; Karim, Zoubida; Muffat-Joly, Martine; Micheli, Laetitia; Eude-Le Parco, Isabelle; Cluzeaud, Françoise; Peuchmaur, Michel; Bonvalet, Jean-Pierre; Poirier, Françoise; Farman, Nicolette Exploring the role of galectin 3 in kidney function: a genetic approach Journal Article In: Glycobiology, vol. 16, no. 1, pp. 36–45, 2006, ISSN: 0959-6658. @article{bichara_exploring_2006,
title = {Exploring the role of galectin 3 in kidney function: a genetic approach},
author = {Bichara, Maurice and Attmane-Elakeb, Amel and Brown, Dennis and Essig, Marie and Karim, Zoubida and Muffat-Joly, Martine and Micheli, Laetitia and Eude-Le Parco, Isabelle and Cluzeaud, Françoise and Peuchmaur, Michel and Bonvalet, Jean-Pierre and Poirier, Françoise and Farman, Nicolette},
doi = {10.1093/glycob/cwj035},
issn = {0959-6658},
year = {2006},
date = {2006-01-01},
journal = {Glycobiology},
volume = {16},
number = {1},
pages = {36--45},
abstract = {Galectin 3 belongs to a family of glycoconjugate-binding proteins that participate in cellular homeostasis by modulating cell growth, adhesion, and signaling. We studied adult galectin 3 null mutant (Gal 3-/-) and wild-type (WT) mice to gain insights into the role of galectin 3 in the kidney. By immunofluorescence, galectin 3 was found in collecting duct (CD) principal and intercalated cells in some regions of the kidney, as well as in the thick ascending limbs at lower levels. Compared to WT mice, Gal 3-/- mice had approximately 11% fewer glomeruli (p textless 0.04), associated with kidney hypertrophy (p textless 0.006). In clearance experiments, urinary chloride excretion was found to be higher in Gal 3-/- than in WT mice (p textless 0.04), but there was no difference in urinary bicarbonate excretion, in glomerular filtration, or urinary flow rates. Under chronic low sodium diet, Gal 3-/- mice had lower extracellular fluid (ECF) volume than WT mice (p textless 0.05). Plasma aldosterone concentration was higher in Gal 3-/- than in WT mice (p textless 0.04), which probably caused the observed increase in alpha-epithelial sodium channel (alpha-ENaC) protein abundance in the mutant mice (p textless 0.001). Chronic high sodium diet resulted paradoxically in lower blood pressure (p textless 0.01) in Gal 3-/- than in WT. We conclude that Gal 3-/- mice have mild renal chloride loss, which causes chronic ECF volume contraction and reduced blood pressure levels.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Galectin 3 belongs to a family of glycoconjugate-binding proteins that participate in cellular homeostasis by modulating cell growth, adhesion, and signaling. We studied adult galectin 3 null mutant (Gal 3-/-) and wild-type (WT) mice to gain insights into the role of galectin 3 in the kidney. By immunofluorescence, galectin 3 was found in collecting duct (CD) principal and intercalated cells in some regions of the kidney, as well as in the thick ascending limbs at lower levels. Compared to WT mice, Gal 3-/- mice had approximately 11% fewer glomeruli (p textless 0.04), associated with kidney hypertrophy (p textless 0.006). In clearance experiments, urinary chloride excretion was found to be higher in Gal 3-/- than in WT mice (p textless 0.04), but there was no difference in urinary bicarbonate excretion, in glomerular filtration, or urinary flow rates. Under chronic low sodium diet, Gal 3-/- mice had lower extracellular fluid (ECF) volume than WT mice (p textless 0.05). Plasma aldosterone concentration was higher in Gal 3-/- than in WT mice (p textless 0.04), which probably caused the observed increase in alpha-epithelial sodium channel (alpha-ENaC) protein abundance in the mutant mice (p textless 0.001). Chronic high sodium diet resulted paradoxically in lower blood pressure (p textless 0.01) in Gal 3-/- than in WT. We conclude that Gal 3-/- mice have mild renal chloride loss, which causes chronic ECF volume contraction and reduced blood pressure levels. |
Romagnoli, P.; Hudrisier, D.; van Meerwijk, J. P. M. Molecular signature of recent thymic selection events on effector and regulatory CD4+ T lymphocytes Journal Article In: Journal of Immunology, vol. 175, pp. 5751-5758, 2005. @article{RN121,
title = {Molecular signature of recent thymic selection events on effector and regulatory CD4+ T lymphocytes},
author = {Romagnoli, P. and Hudrisier, D. and van Meerwijk, J. P. M.},
year = {2005},
date = {2005-01-01},
journal = {Journal of Immunology},
volume = {175},
pages = {5751-5758},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Romagnoli, P.; Tellier, J.; van Meerwijk, J. P. M. Genetic control of thymic development of CD4+CD25+FoxP3+ regulatory T lymphocytes Journal Article In: Eur J Immunol, vol. 35, pp. 3525-3532, 2005. @article{RN123,
title = {Genetic control of thymic development of CD4+CD25+FoxP3+ regulatory T lymphocytes},
author = {Romagnoli, P. and Tellier, J. and van Meerwijk, J. P. M.},
year = {2005},
date = {2005-01-01},
journal = {Eur J Immunol},
volume = {35},
pages = {3525-3532},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Karim, Zoubida; Szutkowska, Marta; Vernimmen, Catherine; Bichara, Maurice Renal handling of NH3/NH4+: recent concepts Journal Article In: Nephron. Physiology, vol. 101, no. 4, pp. p77–81, 2005, ISSN: 1660-2137. @article{karim_renal_2005,
title = {Renal handling of NH3/NH4+: recent concepts},
author = {Karim, Zoubida and Szutkowska, Marta and Vernimmen, Catherine and Bichara, Maurice},
doi = {10.1159/000087575},
issn = {1660-2137},
year = {2005},
date = {2005-01-01},
journal = {Nephron. Physiology},
volume = {101},
number = {4},
pages = {p77--81},
abstract = {To be appropriately excreted in urine, NH4+, the major component of urinary acid excretion, must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Several targets have been identified to account at the gene expression level for the adaptation of renal NH4+ synthesis and transport in response to a chronic acid load. These targets are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) and the Na+/H+(NH4+) exchanger NHE3 in the proximal tubule, the apical Na+-K+(NH4+)-2Cl- cotransporter of the MTAL, the basolateral Na+-K+(NH4+)-2Cl- cotransporter, and likely the epithelial Rh B and C glycoproteins in the collecting ducts. An acid pH per se appears to be a major factor in the control of the expression of these genes during metabolic acidosis probably through activation of pH sensors. Glucocorticoids may also act in concert with an acid pH to coordinate the adaptation of various tubular cell types. The present review focuses on some new aspects of NH3/ NH4+ transport and of regulations of gene expression that have recently emerged.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
To be appropriately excreted in urine, NH4+, the major component of urinary acid excretion, must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Several targets have been identified to account at the gene expression level for the adaptation of renal NH4+ synthesis and transport in response to a chronic acid load. These targets are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) and the Na+/H+(NH4+) exchanger NHE3 in the proximal tubule, the apical Na+-K+(NH4+)-2Cl- cotransporter of the MTAL, the basolateral Na+-K+(NH4+)-2Cl- cotransporter, and likely the epithelial Rh B and C glycoproteins in the collecting ducts. An acid pH per se appears to be a major factor in the control of the expression of these genes during metabolic acidosis probably through activation of pH sensors. Glucocorticoids may also act in concert with an acid pH to coordinate the adaptation of various tubular cell types. The present review focuses on some new aspects of NH3/ NH4+ transport and of regulations of gene expression that have recently emerged. |
Cannarile, M. A.; Decanis, N.; van Meerwijk, J. P.; Brocker, T. The role of dendritic cells in selection of classical and nonclassical CD8+ T cells in vivo Journal Article In: J Immunol, vol. 173, no. 8, pp. 4799-805, 2004. @article{RN120b,
title = {The role of dendritic cells in selection of classical and nonclassical CD8+ T cells in vivo},
author = {Cannarile, M. A. and Decanis, N. and van Meerwijk, J. P. and Brocker, T.},
url = {file://localhost/Users/Joost/Documents/Lab/articles/Cannarile%20JI%202004.pdf},
year = {2004},
date = {2004-01-01},
journal = {J Immunol},
volume = {173},
number = {8},
pages = {4799-805},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
