Evidence map›Paper›PMID 26538236›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

ZnT4 (SLC30A4)-null ("lethal milk") mice have defects in mammary gland secretion and hallmarks of precocious involution during lactation.

Nicholas H McCormick, Sooyeon Lee, Stephen R Hennigar, Shannon L Kelleher

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  5. Article
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  9. Article
  10. Zinc Transporter Proteins.Neurochemical research · 2018
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  12. Zinc in Cellular Regulation: The Nature and Significance of "Zinc Signals".International journal of molecular sciences · 2017
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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

4 authors at 2 institutions in 1 country.

Nicholas H McCormickDepartment of Nutritional Sciences, The Pennsylvania State University, University Park, Pennsylvania.
Sooyeon LeeDepartment of Cellular and Molecular Physiology, Penn State Hershey College of Medicine, Hershey, Pennsylvania;
Stephen R HennigarDepartment of Nutritional Sciences, The Pennsylvania State University, University Park, Pennsylvania.
Shannon L KelleherDepartment of Cellular and Molecular Physiology, Penn State Hershey College of Medicine, Hershey, Pennsylvania; Department of Pharmacology, Penn State Hershey College of Medicine, Hershey, Pennsylvania; Department of Surgery, Penn State Hershey College of Medicine, Hershey, Pennsylvania; and Department of Nutritional Sciences, The Pennsylvania State University, University Park, Pennsylvania slk39@psu.edu.
Pennsylvania State University · USPenn State Milton S. Hershey Medical Center · US

Funding

Intramural NIH HHSPHS HHS D054816
6 · The paper itself

Abstract

During lactation, highly specialized secretory mammary epithelial cells (MECs) produce and secrete huge quantities of nutrients and nonnutritive factors into breast milk. The zinc (Zn) transporter ZnT4 (SLC30A4) transports Zn into the trans-Golgi apparatus for lactose synthesis, and across the apical cell membrane for efflux from MECs into milk. This is consistent with observations in "lethal milk" (lm/lm) mice, which have a truncation mutation in SLC30A4, and present with not only low milk Zn concentration, but also smaller mammary glands, decreased milk volume, and lactation failure by lactation day 2. However, the molecular underpinnings of these defects are not understood. Here, we used lactating C57BL/6J(lm/lm) (ZnT4-null) mice to explore the consequences of a ZnT4-null phenotype on mammary gland function during early lactation. Lactating C57BL/6J(lm/lm) mice had significantly fewer, smaller, and collapsed alveoli comprising swollen, lipid-filled MECs during early lactation. These defects were associated with decreased Akt expression and STAT5 activation, indicative of defects in MEC secretion. In addition, increased expression of ZnT2, TNF-α, and cleaved e-cadherin concomitant with increased activation of STAT3 implicated the loss of ZnT4 in precocious activation of involution. Collectively, our study indicates that the loss of ZnT4 has profound consequences on MEC secretion and may promote tissue remodeling in the mammary gland during early lactation.

Indexed as

AnimalsCadherinsCation Transport ProteinsEpithelial CellsFemaleGenotypeLactationMammary Glands, AnimalMice, Inbred C57BLMice, KnockoutPhenotypeProto-Oncogene Proteins c-aktSignal TransductionSTAT3 Transcription FactorSTAT5 Transcription FactorTime FactorsCadherinsCation Transport ProteinsProto-Oncogene Proteins c-aktSlc30a4 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorSTAT5 Transcription FactorTumor Necrosis Factor-alphalactationmammary glandSLC30A4zincZnT4

Identifiers

PMID26538236
PMCPMC4796636
OpenAlexW2212159349

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.