Changes in cellular composition of kidney collecting duct cells in rats with lithium-induced NDI.

@article{Christensen2004ChangesIC,
  title={Changes in cellular composition of kidney collecting duct cells in rats with lithium-induced NDI.},
  author={B. M. Christensen and D. Marples and Young-hee Kim and Weidong Wang and J. Fr{\o}kiaer and S. Nielsen},
  journal={American journal of physiology. Cell physiology},
  year={2004},
  volume={286 4},
  pages={
          C952-64
        }
}
Lithium treatment for 4 wk caused severe polyuria, dramatic downregulation in aquaporin-2 (AQP-2) expression, and marked decrease in AQP-2 immunoreactivity with the appearance of a large number of cells without AQP-2 labeling in the collecting ducts after lithium treatment. Surprisingly, this was not all due to an increase in AQP-2-negative principal cells, because double immunolabeling revealed that the majority of the AQP-2-negative cells displayed [H(+)]ATPase labeling, which identified them… Expand
Altered expression of selected genes in kidney of rats with lithium-induced NDI.
TLDR
Changes in gene expression are demonstrated not only in the collecting duct but also in the thin limb of the loop of Henle in the IM, and several of these genes are linked to altered sodium and water reabsorption, cell cycling, and changes in interstitial osmolality. Expand
Lithium causes G2 arrest of renal principal cells.
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The data reveal that lithium treatment initiates proliferation of renal principal cells but that a significant percentage of these cells are arrested in the late G2 phase, which explains the reduced principal/intercalated cell ratio and may identify the molecular pathway underlying the development of lithium-induced renal fibrosis. Expand
Evaluation of cellular plasticity in the collecting duct during recovery from lithium-induced nephrogenic diabetes insipidus.
TLDR
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TLDR
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TLDR
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Lithium induces aerobic glycolysis and glutaminolysis in collecting duct principal cells.
TLDR
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Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus.
TLDR
AC6 has a minor role in Li-NDI development but may be important for determining the intercalated cell-to-principal cell ratio, and medullary AQP2 and pS256-AQP2 abundances were lower in AC6loxloxCre mice under standard conditions, and levels were further reduced after Li+ administration. Expand
alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus.
TLDR
The hypothesis that ENaC-mediated lithium entry into the CD principal cells contributes to the pathogenesis of lithium-induced NDI is supported. Expand
Lithium reduces aquaporin-2 transcription independent of prostaglandins.
TLDR
In mpkCCD cells, prostaglandins decrease AQP2 protein stability by increasing its lysosomal degradation, indicating that in vivo paracrine-produced prostag landins might have a role in lithium-induced NDI via this mechanism. Expand
Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats.
TLDR
TAM attenuated polyuria dose dependently and impaired urine concentration and downregulation of AQP2 protein expression in rats with lithium-induced NDI, suggesting that TAM is likely to be a novel therapeutic option for lithium- induces nephrogenic diabetes insipidus. Expand
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