Evidence map›Paper›PMID 35199838›Full record

ArticleMetallomics : integrated biometal science2022

Secretion and uptake of copper via a small copper carrier in blood fluid.

B D Gioilli, T Z Kidane, H Fieten, M Tellez, M Dalphin, A Nguyen, K Nguyen, M C Linder

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

Article in Metallomics : integrated biometal science, 2022. 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
2.3field-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, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Copper Homeostasis and Cuproptosis in Neurological Disorders.Drug design, development and therapy · 2026
    Review
  4. Review
  5. A primer on copper biology in the brain.Neurobiology of disease · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Potential Therapeutic Properties ofPharmaceuticals (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Article
  15. 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

8 authors at 2 institutions in 2 countries.

B D GioilliDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
T Z KidaneDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
H FietenDepartment of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, 3584 CM Utrecht, the Netherlands.
M TellezDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
M DalphinDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
A NguyenDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
K NguyenDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.
M C LinderDepartment of Chemistry and Biochemistry, California State University, 800 N State College Blvd., Fullerton, CA 92834-6866, USA.ORCID 0000-0003-3937-9268
California State University, Fullerton · USUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies with Wilson disease model mice that accumulate excessive copper, due to a dysfunctional ATP7B "copper pump" resulting in decreased biliary excretion, showed that the compensatory increase in urinary copper loss was due to a small copper carrier (∼1 kDa) (SCC). We show here that SCC is also present in the blood plasma of normal and Wilson disease model mice and dogs, as determined by ultrafiltration and size exclusion chromatography (SEC). It is secreted by cultured hepatic and enterocytic cells, as determined by pretreatment with 67Cu nitrilotriacetate (NTA) or nonradioactive 5-10 μM Cu-NTA, and collecting and examining 3 kDa ultrafiltrates of the conditioned media, where a single major copper peak is detected by SEC. Four different cultured cell types exposed to the radiolabeled SCC all took up the 67Cu at various rates. Rates differed somewhat when uptake was from Cu-NTA. Uptake of SCC-67Cu was inhibited by excess nonradioactive Cu(I) or Ag(I) ions, suggesting competition for uptake by copper transporter 1 (CTR1). Knockout of CTR1 in fibroblasts reduced uptake rates by 60%, confirming its participation, but also involvement of other transporters. Inhibitors of endocytosis, or an excess of metal ions taken up by divalent metal transporter 1, did not decrease SCC-67Cu uptake. The results imply that SCC may play a significant role in copper transport and homeostasis, transferring copper particularly from the liver (but also intestinal cells) to other cells within the mammalian organism, as well as spilling excess into the urine in copper overload-as an alternative means of copper excretion.

Indexed as

CopperHepatolenticular DegenerationAnimalsCopper RadioisotopesCopper-Transporting ATPasesDogsMammalsMiceMice, KnockoutCopperCopper-67Copper RadioisotopesCopper-Transporting ATPasesbloodcopper carriersecretionuptakeurine

Identifiers

PMID35199838
PMCPMC8962702
OpenAlexW4213456467

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.