Evidence map›Paper›PMID 26496924›Full record

ArticleHistochemistry and cell biology2016

Aquaporin 2-labeled cells differentiate to intercalated cells in response to potassium depletion.

Wan-Young Kim, Sun Ah Nam, Arum Choi, Yu-Mi Kim, Sang Hee Park, Yong Kyun Kim, Jin Kim

Abstract read
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In one paragraph

Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genes & diseases · 2022
    Article
  5. Renal cystic disease in tuberous sclerosis complex.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  6. Article
  7. Renal-Tubule Epithelial Cell Nomenclature for Single-Cell RNA-Sequencing Studies.Journal of the American Society of Nephrology : JASN · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Wan-Young KimDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea.
Sun Ah NamDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea.
Arum ChoiDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea.
Yu-Mi KimDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea.
Sang Hee ParkInstitute of Clinical Medicine Research of Bucheon St. Mary's Hospital, Bucheon-si, Korea.
Yong Kyun KimDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea. drkimyk@catholic.ac.kr.
Jin KimDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul, 137-701, Korea. jinkim@catholic.ac.kr.
Catholic University of Korea · KRThe Catholic University of Korea Bucheon St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian renal collecting duct consists of principal cells (PCs) and intercalated cells (ICs). Both PCs and ICs are involved in potassium (K(+)) homeostasis, PCs through their role in K(+) secretion and ICs through their ability to facilitate K(+) resorption. We previously hypothesized that PCs may differentiate into ICs upon K(+) depletion. However, no direct evidence has yet been obtained to conclusively demonstrate that PCs differentiate into ICs in response to K(+) depletion. Here, we present direct evidence for the differentiation of PCs into ICs by cell lineage tracing using aquaporin 2 (AQP2)-Cre mice and R26R-EYFP transgenic mice. In control mice, AQP2-EYFP(+) cells exhibited mainly a PC phenotype (AQP2-positive/H(+)-ATPase-negative). Interestingly, some AQP2-EYFP(+) cells exhibited an IC phenotype (H(+)-ATPase-positive/AQP2-negative); these cells accounted for 1.7 %. After K(+) depletion, the proportion of AQP2-EYFP(+) cells with an IC phenotype was increased to 4.1 %. Furthermore, some AQP2-EYFP(+) cells exhibited a "null cell" phenotype (AQP2-negative/H(+)-ATPase-negative) after K(+) depletion. Collectively, our data demonstrate that AQP2-labeled cells can differentiate into ICs, as well as null cells, in response to K(+) depletion. This finding indicates that some of AQP2-labeled cells possess properties of progenitor cells and that they can differentiate into ICs in the adult mouse kidney.

Indexed as

AnimalsAquaporin 2Bacterial ProteinsCell DifferentiationCell LineageCells, CulturedEpithelial CellsKidney Tubules, CollectingLuminescent ProteinsMiceMice, KnockoutPotassiumAqp2 protein, mouseAquaporin 2Bacterial ProteinsLuminescent ProteinsPotassiumyellow fluorescent protein, BacteriaAquaporinDifferentiationIntercalated cellsPrincipal cell

Identifiers

PMID26496924
OpenAlexW1820369890

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.