Evidence map›Paper›PMID 23308014›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

Aqp2-expressing cells give rise to renal intercalated cells.

Hongyu Wu, Lihe Chen, Qiaoling Zhou, Xi Zhang, Stefan Berger, Jiong Bi, Dorothy E Lewis, Yang Xia, Wenzheng Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 84 citations in OpenAlex.

  1. Hmx2 and Dmrt2 Coordinate the Differentiation of Intercalated Cell Subtypes in Kidney.Journal of the American Society of Nephrology : JASN · 2026
    Article
  2. Role of KThe American journal of pathology · 2025
    Article
  3. Kidney Disease Modeling with Organoids and Organs-on-Chips.Annual review of biomedical engineering · 2024
    Review
  4. Intercalated cell function, kidney innate immunity, and urinary tract infections.Pflugers Archiv : European journal of physiology · 2024
    Review
  5. Article
  6. Article
  7. Generation ofAmerican journal of physiology. Renal physiology · 2023
    Article
  8. Absence of E-Cadherin and β-Catenin in the Basal Plasma Membrane of Collecting Duct Cells During NDI Development and Recovery.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023
    Article
  9. Article
  10. NaHypertension (Dallas, Tex. : 1979) · 2022
    Article
  11. Review
  12. Potential renal stem/progenitor cells identified by in vivo lineage tracing.American journal of physiology. Renal physiology · 2022
    Review
  13. The Role of Histone H3 Methylation in Acute Kidney Injury.Drug design, development and therapy · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Hongyu WuDepartment of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, Texas, USA.
Lihe Chen
Qiaoling Zhou
Xi Zhang
Stefan Berger
Jiong Bi
Dorothy E Lewis
Yang Xia
Wenzheng Zhang
The University of Texas Health Science Center at Houston · USCentral South University · CNGerman Cancer Research Center · DE

Funding

Epigenic Control of ENaC Transcription and Sodium TransportR01DK080236 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ZHANG, WENZHENG · 2009 to 2016
$2.2M
Metabolites, Sickle Cell Disease, and Novel TherapeuticsR01HL113574 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI XIA, YANG · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL113574NIDDK NIH HHS R01 DK080236
6 · The paper itself

Abstract

The mammalian collecting duct comprises principal and intercalated cells, which maintain sodium/water and acid/base balance, respectively, but the epigenetic contributors to the differentiation of these cell types remain unknown. Here, we investigated whether the histone H3 K79 methyltransferase Dot1l, which is highly expressed in principal cells, participates in this process. Taking advantage of the distribution of aquaporin 2 (Aqp2), which localizes to principal cells of the collecting duct, we developed mice lacking Dot1l in Aqp2-expressing cells (Dot1l(AC)) and found that these mice had approximately 20% fewer principal cells and 13%-16% more intercalated cells than control mice. This deletion of Dot1l in principal cells abolished histone H3 K79 methylation in these cells, but unexpectedly, most intercalated cells also had undetectable di-methyl K79, suggesting that Aqp2(+) cells give rise to intercalated cells. These Aqp2(+) cell-derived intercalated cells were present in both developing and mature kidneys. Furthermore, compared with control mice, Dot1l(AC) mice had 40% higher urine volume and 18% lower urine osmolarity with relatively normal electrolyte and acid-base homeostasis. In conclusion, these data suggest that Dot1l deletion facilitates the differentiation of some α- and β-intercalated cells from Aqp2-expressing progenitor cells or mature principal cells.

Indexed as

Acid-Base ImbalanceAnimalsAquaporin 2Cell DifferentiationCell LineageEpigenesis, GeneticFemaleHistone-Lysine N-MethyltransferaseHistonesIntegrasesKidney Tubules, CollectingMaleMethylationMethyltransferasesMiceMice, Inbred C57BLAqp2 protein, mouseAquaporin 2Cre recombinaseDot1l protein, mouseHistone-Lysine N-MethyltransferaseHistonesIntegrasesMethyltransferases

Identifiers

PMID23308014
PMCPMC3559490
OpenAlexW2129408106

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.