scholarly journals Transcription Factor Elf3 Modulates Vasopressin-Induced Aquaporin-2 Gene Expression in Kidney Collecting Duct Cells

2019 ◽  
Vol 10 ◽  
Author(s):  
Shu-Ting Lin ◽  
Chia-Ching Ma ◽  
Kuang-Ting Kuo ◽  
Yin-Fang Su ◽  
Wei-Ling Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Collecting Duct ◽  
Kidney Collecting Duct ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells

scholarly journals FP027VASOPRESSIN-REGULATED MICRORNAS AND AQUAPORIN-2-TARGETING MICRORNAS IN KIDNEY COLLECTING DUCT CELLS

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii74-iii74
Author(s):  
Tae-Hwan Kwon ◽  
Jae-Eun Kim ◽  
Hyun Jun Jung ◽  
Yu-Jung Lee
Keyword(s):  
Collecting Duct ◽  
Kidney Collecting Duct ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells

MAGED2 controls vasopressin-induced aquaporin-2 expression in collecting duct cells

2021 ◽  
pp. 104424
Author(s):  
Björn Reusch ◽  
Malte P. Bartram ◽  
Claudia Dafinger ◽  
Nicolàs Palacio-Escat ◽  
Andrea Wenzel ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells

AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5′-flanking region of the VIT32 gene

2004 ◽  
Vol 287 (3) ◽  
pp. F460-F468 ◽  
Author(s):  
Christie P. Thomas ◽  
Randy W. Loftus ◽  
Kang Z. Liu
Keyword(s):  
Gene Expression ◽  
Promoter Region ◽  
Collecting Duct ◽  
Airway Epithelial Cells ◽  
Proximal Promoter ◽  
Xenopus Laevis Oocytes ◽  
Proximal Promoter Region ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Flanking Region

VIT32, a vasopressin-induced transcript, inhibits Na+ transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes ( EMBO J 21: 5109–5117, 2002). To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells. Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h. The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription. An ∼1.5-kb fragment of the 5′-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells. By deletion analysis and site-directed mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP. Furthermore, DDAVP-stimulated VIT32 promoter-reporter activity was inhibited by H89 and by a dominant negative CREB construct. Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays. In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene.

scholarly journals Lixivaptan, a New Generation Diuretic, Counteracts Vasopressin-Induced Aquaporin-2 Trafficking and Function in Renal Collecting Duct Cells

2019 ◽  
Vol 21 (1) ◽  
pp. 183
Author(s):  
Annarita Di Mise ◽  
Maria Venneri ◽  
Marianna Ranieri ◽  
Mariangela Centrone ◽  
Lorenzo Pellegrini ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Water Channel ◽  
Plasma Osmolality ◽  
Kinetic Measurements ◽  
Aquaporin 2 ◽  
Plasma Vasopressin ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Renal Collecting Duct ◽  
New Generation

Vasopressin V2 receptor (V2R) antagonists (vaptans) are a new generation of diuretics. Compared with classical diuretics, vaptans promote the excretion of retained body water in disorders in which plasma vasopressin concentrations are inappropriately high for any given plasma osmolality. Under these conditions, an aquaretic drug would be preferable over a conventional diuretic. The clinical efficacy of vaptans is in principle due to impaired vasopressin-regulated water reabsorption via the water channel aquaporin-2 (AQP2). Here, the effect of lixivaptan—a novel selective V2R antagonist—on the vasopressin-cAMP/PKA signaling cascade was investigated in mouse renal collecting duct cells expressing AQP2 (MCD4) and the human V2R. Compared to tolvaptan—a selective V2R antagonist indicated for the treatment of clinically significant hypervolemic and euvolemic hyponatremia—lixivaptan has been predicted to be less likely to cause liver injury. In MCD4 cells, clinically relevant concentrations of lixivaptan (100 nM for 1 h) prevented dDAVP-induced increase of cytosolic cAMP levels and AQP2 phosphorylation at ser-256. Consistent with this finding, real-time fluorescence kinetic measurements demonstrated that lixivaptan prevented dDAVP-induced increase in osmotic water permeability. These data represent the first detailed demonstration of the central role of AQP2 blockade in the aquaretic effect of lixivaptan and suggest that lixivaptan has the potential to become a safe and effective therapy for the treatment of disorders characterized by high plasma vasopressin concentrations and water retention.

Adaptation to alkalosis induces cell cycle delay and apoptosis in cortical collecting duct cells: Role of aquaporin-2

2010 ◽  
Vol 224 (2) ◽  
pp. 405-413 ◽  
Author(s):  
Valeria Rivarola ◽  
Pilar Flamenco ◽  
Luciana Melamud ◽  
Luciano Galizia ◽  
Paula Ford ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Cell Cycle Delay ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells
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