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Am J Physiol Renal Physiol (January 24, 2006). doi:10.1152/ajprenal.00383.2005
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Submitted on September 23, 2005
Accepted on January 19, 2006

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

Birgitte Monster Christensen1, Young-Hee Kim1, Tae-Hwan Kwon2, and Soren Nielsen1*

1 The Water and Salt Research Center, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C, Denmark
2 The Water and Salt Research Center, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C, Denmark; Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu 700-422, Korea, Democratic People's Rep

* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.

Lithium (Li) treatment for 4 weeks has previously been shown to increase the fraction of intercalated cells in parallel with a decrease in the fraction of principal cells in the kidney collecting duct (6, 14). To study how early this fractional change starts, the origin of the cells and the possible mechanism behind the changes, we did time-course studies in rats subjected to different durations of Li treatment (i.e., for 4, 10 and 15 days). Increased urine output was already observed at day 4 of Li treatment with decreased AQP2 levels although not statistically significant. At day 10 and 15 both a significant polyuria and downregulation in AQP2 expression were observed. At day 10, the density of H+-ATPase-positive cells was increased in the IMCD of Li-treated rats and this was further pronounced at day 15. Some of the H+-ATPase positive cells did not co-stain with Cl-/HCO3- exchanger AE1 indicating that they were not fully differentiated to type A IC. By double-labelling for either H+-ATPase and proliferating cell nuclear antigen (PCNA) or for AQP4 and PCNA, we found that proliferation mainly occurred in proximal IMCD cells at day 4 and it increased toward the middle part of the IMCD in response to prolonged Li treatment. Most cells expressing PCNA were stained with AQP4 but not with H+-ATPase. Triple-labeling for H+-ATPase, AQP4 and PCNA showed a subset of cells negative for all three proteins or only positive for PCNA. In contrast, a four week-recovery period after 4 weeks of Li treatment reversed the enhanced proliferative rate to the control levels. In conclusion, 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. This is likely to contribute to the remodelling of the collecting duct after Li treatment.




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