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

Role of AQP2 during apoptosis in cortical collecting duct cells

2009 ◽  
Vol 101 (4) ◽  
pp. 237-250 ◽  
Author(s):  
Pilar Flamenco ◽  
Luciano Galizia ◽  
Valeria Rivarola ◽  
Juan Fernandez ◽  
Paula Ford ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Duct Cells ◽  
Collecting Duct Cells

Chloroquine attenuates lithium-induced NDI and proliferation of renal collecting duct cells

2020 ◽  
Vol 318 (5) ◽  
pp. F1199-F1209 ◽  
Author(s):  
Yang Du ◽  
Yun Qian ◽  
Xiaomei Tang ◽  
Yan Guo ◽  
Shuang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Collecting Duct ◽  
Mammalian Target Of Rapamycin ◽  
Duct Cell ◽  
Nuclear Antigen ◽  
Kidney Cortex ◽  
Cortical Collecting Duct ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells

Lithium is widely used in psychiatry as the golden standard for more than 60 yr due to its effectiveness. However, its adverse effect has been limiting its long-term use in clinic. About 40% of patients taking lithium develop nephrogenic diabetes insipidus (NDI). Lithium can also induce proliferation of collecting duct cells, leading to microcyst formation in the kidney. Lithium was considered an autophagy inducer that might contribute to the therapeutic benefit of neuropsychiatric disorders. Thus, we hypothesized that autophagy may play a role in lithium-induced kidney nephrotoxicity. To address our hypothesis, we fed mice with a lithium-containing diet with chloroquine (CQ), an autophagy inhibitor, concurrently. Lithium-treated mice presented enhanced autophagy activity in the kidney cortex and medulla. CQ treatment significantly ameliorated lithium-induced polyuria, polydipsia, natriuresis, and kaliuresis accompanied with attenuated downregulation of aquaporin-2 and Na+-K+-2Cl− cotransporter protein. The protective effect of CQ on aquaporin-2 protein abundance was confirmed in cultured cortical collecting duct cells. In addition, we found that lithium-induced proliferation of collecting duct cells was also suppressed by CQ as detected by proliferating cell nuclear antigen staining. Moreover, both phosphorylated mammalian target of rapamycin and β-catenin expression, which have been reported to be increased by lithium and associated with cell proliferation, were reduced by CQ. Taken together, our study demonstrated that CQ protected against lithium-induced NDI and collecting duct cell proliferation possibly through inhibiting autophagy.

scholarly journals Exosomal transmission of functional aquaporin 2 in kidney cortical collecting duct cells

2011 ◽  
Vol 589 (24) ◽  
pp. 6119-6127 ◽  
Author(s):  
Jonathan M. Street ◽  
Willem Birkhoff ◽  
Robert I. Menzies ◽  
David J. Webb ◽  
Matthew A. Bailey ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Aquaporin 2 ◽  
Duct Cells ◽  
Collecting Duct Cells

scholarly journals The Angiotensin II Type 1 Receptor-Associated Protein Attenuates Angiotensin II-Mediated Inhibition of the Renal Outer Medullary Potassium Channel in Collecting Duct Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Juliano Zequini Polidoro ◽  
Nancy Amaral Rebouças ◽  
Adriana Castello Costa Girardi
Keyword(s):  
Angiotensin Ii ◽  
Cell Surface ◽  
Collecting Duct ◽  
Cell Surface Expression ◽  
Ang Ii ◽  
Cortical Collecting Duct ◽  
Duct Cells ◽  
Collecting Duct Cells

Adjustments in renal K+ excretion constitute a central mechanism for K+ homeostasis. The renal outer medullary potassium (ROMK) channel accounts for the major K+ secretory route in collecting ducts during basal conditions. Activation of the angiotensin II (Ang II) type 1 receptor (AT1R) by Ang II is known to inhibit ROMK activity under the setting of K+ dietary restriction, underscoring the role of the AT1R in K+ conservation. The present study aimed to investigate whether an AT1R binding partner, the AT1R-associated protein (ATRAP), impacts Ang II-mediated ROMK regulation in collecting duct cells and, if so, to gain insight into the potential underlying mechanisms. To this end, we overexpressed either ATRAP or β-galactosidase (LacZ; used as a control), in M-1 cells, a model line of cortical collecting duct cells. We then assessed ROMK channel activity by employing a novel fluorescence-based microplate assay. Experiments were performed in the presence of 10−10 M Ang II or vehicle for 40 min. We observed that Ang II-induced a significant inhibition of ROMK in LacZ, but not in ATRAP-overexpressed M-1 cells. Inhibition of ROMK-mediated K+ secretion by Ang II was accompanied by lower ROMK cell surface expression. Conversely, Ang II did not affect the ROMK-cell surface abundance in M-1 cells transfected with ATRAP. Additionally, diminished response to Ang II in M-1 cells overexpressing ATRAP was accompanied by decreased c-Src phosphorylation at the tyrosine 416. Unexpectedly, reduced phospho-c-Src levels were also found in M-1 cells, overexpressing ATRAP treated with vehicle, suggesting that ATRAP can also downregulate this kinase independently of Ang II-AT1R activation. Collectively, our data support that ATRAP attenuates inhibition of ROMK by Ang II in collecting duct cells, presumably by reducing c-Src activation and blocking ROMK internalization. The potential role of ATRAP in K+ homeostasis and/or disorders awaits further investigation.

Hormone-regulated transepithelial Na+ transport in mammalian CCD cells requires SGK1 expression

2003 ◽  
Vol 284 (3) ◽  
pp. F480-F487 ◽  
Author(s):  
My N. Helms ◽  
Géza Fejes-Tóth ◽  
Anikó Náray-Fejes-Tóth
Keyword(s):  
Mammalian Cells ◽  
Collecting Duct ◽  
Full Length ◽  
Cortical Collecting Duct ◽  
Dexamethasone Treatment ◽  
Duct Cells ◽  
High Insulin ◽  
Collecting Duct Cells ◽  
Phox Homology

To study the role of serum and glucocorticoid-inducible kinase-1 (SGK1) in mammalian cells, we compared Na+ transport rates in wild-type (WT) M1 cortical collecting duct cells with M1 populations stably expressing human full-length SGK1, NH2-terminal truncated (ΔN-60) SGK1, “kinase-dead” (K127M) SGK1, and cells that have downregulated levels of SGK1 mRNA (antisense SGK1). Basal rates of transepithelial Na+ transport were highest in full-length SGK1 populations, compared among the above populations. Dexamethasone treatment increased Na+ transport in WT and full-length SGK1 cells 2.7- and 2-fold, respectively. Modest stimulation of Na+ absorption was detected after dexamethasone treatment in ΔN-60 SGK1 populations. However, ΔN-60 SGK1 transport rates remained substantially lower than WT values. Importantly, a combination of high insulin, dexamethasone, and serum failed to significantly stimulate Na+ transport in antisense or K127M SGK1 cells. Additionally, expression of antisense SGK1 significantly decreased transepithelial resistance values. Overall, we concluded that SGK1 is a critical component in corticosteroid-regulated Na+ transport in mammalian cortical collecting duct cells. Furthermore, our data suggest that the NH2 terminus of SGK1 may contain a Phox homology-like domain that may be necessary for effective Na+transport.

Volume regulation in cortical collecting duct cells: role of AQP2

2005 ◽  
Vol 97 (9) ◽  
pp. 687-697 ◽  
Author(s):  
Paula Ford ◽  
Valeria Rivarola ◽  
Osvaldo Chara ◽  
Marcel Blot-Chabaud ◽  
Françoise Cluzeaud ◽  
...  
Keyword(s):  
Volume Regulation ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Duct Cells ◽  
Collecting Duct Cells

Whole cell and unitary amiloride-sensitive sodium currents in M-1 mouse cortical collecting duct cells

1996 ◽  
Vol 270 (4) ◽  
pp. C998-C1010 ◽  
Author(s):  
M. L. Chalfant ◽  
T. G. O'Brien ◽  
M. M. Civan
Keyword(s):  
Collecting Duct ◽  
Cell Permeability ◽  
Na Channel ◽  
Na Channels ◽  
Cortical Collecting Duct ◽  
Ionic Selectivity ◽  
Whole Cell ◽  
Duct Cells ◽  
Excised Patches ◽  
Collecting Duct Cells

Amiloride-sensitive whole cell currents have been reported in M-1 mouse cortical collecting duct cells (Korbmacher et al., J. Gen. Physiol. 102: 761-793, 1993). We have confirmed that amiloride inhibits the whole cell currents but not necessarily the measured whole cell currents. Anomalous responses were eliminated by removing external Na+ and/or introducing paraepithelial shunts. The amiloride-sensitive whole cell currents displayed Goldman rectification. The ionic selectivity sequence of the amiloride-sensitive conductance was Li+ > Na+ >> K+. Growth of M-1 cells on permeable supports increased the amiloride-sensitive whole cell permeability, compared with cells grown on plastic. Single amiloride-sensitive channels were observed, which conformed to the highly selective low-conductance amiloride-sensitive class [Na(5)] of epithelial Na+ channels. Hypotonic pretreatment markedly slowed run-down of channel activity. The gating of the M-1 Na+ channel in excised patches was complex. Open- and closed-state dwell-time distributions from patches that display one operative channel were best described with two or more exponential terms each. We conclude that 1) study of M-1 whole cell Na+ currents is facilitated by reducing the transepithelial potential to zero, 2) these M-1 currents reflect the operation of Na(5) channels, and 3) the Na+ channels display complex kinetics, involving > or = 2 open and > or = 2 closed states.

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
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