@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}

}

@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}

}

@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}

}

@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}

}

@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}

}

@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}

}

@article{RN118,

title = {Induction of antigen-specific tolerance to bone-marrow allografts with CD4+CD25+ T lymphocytes},

author = {Joffre, O. and Gorsse, N. and Romagnoli, P. and Hudrisier, D. and van Meerwijk, J. P.M.},

url = {file://D:%5CJoost's%20files%5Cmanuscripts%5CBlood%202004%20(Treg%20BM%20transplantation)%5CBlood%20submission%5Cresubmission%5CJoffre%20et%20al.pdf},

year  = {2004},

date = {2004-01-01},

journal = {Blood},

volume = {103},

number = {11},

pages = {4216-4221},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{karim_acid_2003,

title = {Acid pH increases the stability of BSC1/NKCC2 mRNA in the medullary thick ascending limb},

author = {Karim, Zoubida and Attmane-Elakeb, Amel and Sibella, Valérie and Bichara, Maurice},

doi = {10.1097/01.asn.0000085023.73801.4a},

issn = {1046-6673},

year  = {2003},

date = {2003-09-01},

journal = {Journal of the American Society of Nephrology: JASN},

volume = {14},

number = {9},

pages = {2229--2236},

abstract = {Chronic metabolic acidosis enhances the ability of the medullary thick ascending limb (MTAL) to absorb NH(4)(+) at least in part by stimulating the mRNA and protein expression of BSC1/NKCC2, the MTAL apical Na(+)-K(+)(NH(4)(+))-2Cl(-) co-transporter. For assessing the mechanism by which an acid pH enhances the BSC1 mRNA abundance, MTAL were harvested from adrenalectomized rats and incubated in control (pH 7.35) and acid (pH 7.10) 1:1 mixtures of Ham's nutrient mixture F-12 and DME. rBSC1 mRNA abundance and gene transcription rate were quantified by quantitative reverse transcription-PCR and run-off assay, respectively. Acid incubation enhanced mRNA abundance within 4 h in whole cell (P textless 0.02) but not in nucleus. BSC1 gene transcription rate was not affected by acid incubation. In contrast, under conditions in which gene transcription was blocked, rBSC1 mRNA decreased within 6 h by 38 +/- 11% in control but only by 15 +/- 15% in acid medium (P textless 0.02), which represented an increase in the BSC1 mRNA half-life from approximately 7 to approximately 17 h. Furthermore, in a mouse TAL cell line, acid incubation for 16 h significantly increased (P textless 0.02) the amount of BSC1 mRNA in cells transfected with the full-length mBSC1 cDNA but not in cells transfected with a mBSC1 cDNA lacking the 3'-UTR. These results demonstrate that acid pH enhances the stability of BSC1 mRNA probably by activating pathways that act on the AU-rich 3'-UTR of BSC1 mRNA, which contributes to the renal response to metabolic acidosis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN114,

title = {Selective absence of CD8+ TCRalpha beta+ intestinal epithelial cells in transgenic mice expressing beta2-microglobulin-associated ligands exclusively on thymic cortical epithelium.},

author = {Capone, M. and Lees, R.L. and Finke, D. and Ernst, B. and van Meerwijk, J. P. M. and MacDonald, H. R.},

url = {D:Joost's filesarticlesCapone EJI 2003.pdf},

year  = {2003},

date = {2003-01-01},

journal = {Eur J Immunol},

volume = {33},

number = {6},

pages = {1471-7},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN115,

title = {Oxidative stress-induced T lymphocyte hyporesponsiveness is caused by structural modification rather than proteasomal degradation of crucial signaling molecules},

author = {Cemerski, S. and van Meerwijk, J.P.M. and Romagnoli, P.},

year  = {2003},

date = {2003-01-01},

journal = {Eur J Immunol},

volume = {33},

number = {8},

pages = {2178-85},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN108b,

title = {In vivo maintenance of T lymphocyte unresponsiveness induced by thymic medullary epithelium requires antigen presentation by radioresistant cells},

author = {Hudrisier, D. and Feau, S. and Bonnet, V. and Romagnoli, P. and van Meerwijk, J.P.M.},

year  = {2003},

date = {2003-01-01},

journal = {Immunology},

volume = {108},

pages = {24-31},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{karim_renal_2002,

title = {Renal handling of NH4+ in relation to the control of acid-base balance by the kidney},

author = {Karim, Zoubida and Attmane-Elakeb, Amel and Bichara, Maurice},

issn = {1121-8428},

year  = {2002},

date = {2002-04-01},

journal = {Journal of Nephrology},

volume = {15 Suppl 5},

pages = {S128--134},

abstract = {The major component of urinary acid excretion is NH4+. To be appropriately excreted in urine, NH4+ 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. Each step of this renal pathway is highly regulated and, in addition to acute events mediated by peptide hormones such as parathyroid hormone, the control of gene expression explains how the renal handling of NH4+ fully adapts to chronic changes in the acid-base status. Several targets have been identified at the gene expression level to account for the adaptation of renal NH4+ synthesis and transport in response to an acid load. These are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) in the proximal tubule, the apical Na(+)-K+(NH4+)-2Cl- cotransporter of the MTAL, and the basolateral Na(+)-K+(NH4+)-2Cl- cotransporter of medullary collecting ducts. At least two factors control the expression of these genes during metabolic acidosis: an acid pH and glucocorticoids, which appear to act in concert to coordinate the adaptation of various tubular cell types. The present review focuses on some aspects of these regulations that have been recently elucidated.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN106,

title = {Reactive oxygen species differentially affect T cell receptor signaling pathways},

author = {Cemerski, S. and Cantagrel, A. and van Meerwijk, J. P.M. and Romagnoli, P.},

url = {D:Joost's filesarticlesCemerski JBC 2002.pdf},

year  = {2002},

date = {2002-01-01},

journal = {Journal of Biological Chemistry},

volume = {277},

pages = {19585-19593},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN126,

title = {Collagenase-1 (MMP-1) and HLA-DRB1 gene polymorphisms in rheumatoid arthritis: a prospective longitudinal study},

author = {Constantin, A. and Lauwers-Cances, V. and Navaux, F. and Abbal, M. and van Meerwijk, J. and Mazieres, B. and Cambon-Thomsen, A. and Cantagrel, A.},

url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11824952},

year  = {2002},

date = {2002-01-01},

journal = {J Rheumatol},

volume = {29},

number = {1},

pages = {15-20},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN125,

title = {Stromelysin 1 (matrix metalloproteinase 3) and HLA-DRB1 gene polymorphisms: Association with severity and progression of rheumatoid arthritis in a prospective study},

author = {Constantin, A. and Lauwers-Cances, V. and Navaux, F. and Abbal, M. and van Meerwijk, J. and Mazieres, B. and Cambon-Thomsen, A. and Cantagrel, A.},

url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12124858},

year  = {2002},

date = {2002-01-01},

journal = {Arthritis Rheum},

volume = {46},

number = {7},

pages = {1754-62},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN103,

title = {Preferential recognition of self-antigens despite normal thymic deletion of CD4+CD25+ regulatory T cells},

author = {Romagnoli, P. and Hudrisier, D. and van Meerwijk, J.P.M.},

url = {D:Joost's filesarticlesRomagnoli JI 2002.pdf},

year  = {2002},

date = {2002-01-01},

journal = {Journal of Immunology},

volume = {168},

pages = {1644-1648},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN91,

title = {A potential role for tyrosine kinase p56lck in rheumatoid arthritis synovial fluid T lymphocyte hyporesponsiveness},

author = {Romagnoli, P. and Strahan, D. and Pelosi, M. and Cantagrel, A. and van Meerwijk, J.P.M.},

year  = {2001},

date = {2001-01-01},

journal = {International Immunology},

volume = {13},

number = {3},

pages = {305-312},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{noauthor_notitle_nodate,

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{d,

title = {(No Title)},

url = {http://science.sciencemag.org/},

doi = {10.1126/science.abf2022},

keywords = {},

pubstate = {published},

tppubtype = {article}

}