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={Birgitte M. Christensen and David D.R. Marples and Young-Hee Kim and Weidong Wang and J{\o}rgen Fr{\o}kiaer and S{\o}ren Steen Nielsen},
  journal={American journal of physiology. Cell physiology},
  year={2004},
  volume={286 4},
  pages={
          C952-64
        },
  url={https://api.semanticscholar.org/CorpusID:20227998}
}
Lithium treatment not only decreased AQP-2 expression, but dramatically and reversibly reduced the fraction of principal cells and altered the cellular organization in collecting ducts, likely to be important in lithium-induced nephrogenic diabetes insipidus.
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Altered expression of selected genes in kidney of rats with lithium-induced NDI.

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.

Lithium causes G2 arrest of renal principal cells.

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.

Evaluation of cellular plasticity in the collecting duct during recovery from lithium-induced nephrogenic diabetes insipidus.

This study has identified for the first time, in vivo, a novel cellular type positive for both intercalated and principal cells functional markers, as recognized by colabeling with H(+)-ATPase/aquaporin-4 (AQP4) and anion exchanger-1 (AE-1)/AqP2 and Foxi1/AQp4.

Chronic lithium treatment induces novel patterns of pendrin localization and expression.

Observations suggest that renal IMCD cell plasticity may play an important role in lithium-induced IMCD remodeling, including a novel phenotype wherein pendrin was coexpressed with aquaporin-4.

Lithium treatment induces a marked proliferation of primarily principal cells in rat kidney inner medullary collecting duct.

The Li-induced increase in the density of intercalated cells is associated with a high proliferative rate of principal cells in the IM-1 and IM-2 rather than a selective proliferation of interCalated cells as expected.

Lithium induces aerobic glycolysis and glutaminolysis in collecting duct principal cells.

Together, the data reveal that lithium induces aerobic glycolysis and glutaminolysis in principal cells and that inhibition of aerobic glyCOlysis, but not the glutaminosynthesis, does not attenuate Li-NDI.

Tamoxifen Affects Aquaporin-3 Expression and Subcellular Localization in Rat and Human Renal Collecting Ducts

It is suggested that TAM attenuates the downregulation of AQP3 in a UUO model and a lithium-induced NDI model and affects the intracellular localization in the collecting ducts.

Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus.

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.

alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus.

The hypothesis that ENaC-mediated lithium entry into the CD principal cells contributes to the pathogenesis of lithium-induced NDI is supported.

Lithium reduces aquaporin-2 transcription independent of prostaglandins.

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.
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44 References

Altered expression of renal acid-base transporters in rats with lithium-induced NDI.

Results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment, likely to represent direct or compensatory effects to increase the capacity for HCO3- re absorption, NH4+ reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.

Lithium-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla.

Lithium causes marked downregulation of AQP2 expression, only partially reversed by cessation of therapy, thirsting or dDAVP treatment, consistent with clinical observations of slow recovery from lithium-induced urinary concentrating defects.

Altered expression of renal AQPs and Na(+) transporters in rats with lithium-induced NDI.

Severe downregulation of AQP2 and AQP3 appears to be important for the development of Li-induced polyuria, while the increased or unchanged expression of NHE3, BSC-1, Na-K-ATPase, and TSC indicates that these Na(+) transporters do not participate in the developmentof Li- induced polyuria.

Remodeling the cellular profile of collecting ducts by chronic carbonic anhydrase inhibition.

The cellular profile of the collecting ducts of adult rats can be remodeled by inhibiting CA activity in rats by using osmotic pumps containing acetazolamide, suggesting that CA activity plays an important role in determining the differentiated phenotype of medullary collecting duct epithelial cells.

Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats.

The results strongly suggest that AQP2 downregulation and reduced apical plasma membrane delivery of AQP1 play important roles in the development of polyuria in association with hypercalcemia.

Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex.

Hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level ofpolyuria induced, supporting the view that there is a causative link.

Axial heterogeneity in basolateral AQP2 localization in rat kidney: effect of vasopressin.

There was no increase in AQP2 labeling of the BLM in response to short-term dDAVP, and acute V(2)-receptor antagonist treatment did not cause retrieval of AQP 2 from the BLM.

Downregulation of aquaporin-2 parallels changes in renal water excretion in unilateral ureteral obstruction.

In bilateral ureteral obstruction, both aquaporin-2 (AQP2) levels and urinary concentrating capacity are markedly reduced, which together with the reduced expression and elevated free water clearance strongly suggests a role of AQP2 in the observed compensatory diuresis from nonobstructed kidneys.

Aquaporin-3 water channel localization and regulation in rat kidney.

Investigating the localization and regulation in the kidney of peptide-derived, affinity-purified polyclonal antibody to aquaporin-3 found that the expression of AQP-3 is regulated on a long-term basis, suggesting that this water channel is not regulated acutely through vesicular trafficking.

Vasopressin-elicited water and urea permeabilities are altered in IMCD in hypercalcemic rats.

It is concluded that selective alterations in IMCD transport occur in hypercalcemia, permitting the body to dispose of excess calcium without forming calcium-containing renal stones.