Evidence map›Paper›PMID 35892685›Full record

ArticleBiomedicines2022

Vitamin D-Dimer: A Possible Biomolecule Modulator in Cytotoxic and Phagocytosis Processes?

Ralf Herwig, Katharina Erlbacher, Amela Ibrahimagic, Mehtap Kacar, Naime Brajshori, Petrit Beqiri, Joachim Greilberger

Abstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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.

Ralf HerwigLaboratories PD Dr. R. Herwig, 80337 Munich, Germany.ORCID 0000-0002-9879-6742
Katharina ErlbacherLaboratories PD Dr. R. Herwig, 80337 Munich, Germany.
Amela IbrahimagicDepartment of Speech and Language Pathology and Audiology, Faculty of Education and Rehabilitation, University of Tuzla, 75000 Tuzla, Bosnia and Herzegovina.ORCID 0000-0002-2786-8884
Mehtap KacarDepartment of Physiology, Faculty of Medicine, Yeditepe University, Ataşehir, 34755 İstanbul, Turkey.ORCID 0000-0002-1572-4787
Naime BrajshoriHeimerer-College, 10000 Pristina, Kosovo.
Petrit BeqiriHeimerer-College, 10000 Pristina, Kosovo.
Joachim GreilbergerInstitut fuer Laborwissenschaften, 8301 Lassnitzhoehe, Austria.ORCID 0000-0001-6676-0908

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Vitamin D3 complexed to deglycosylated vitamin D binding protein (VitD-dgVDBP) is a water-soluble vitamin D dimeric compound (VitD-dgVDBP). It is not clear how VitD-dgVDBP affects circulating monocytes, macrophages, other immune cell systems, including phagocytosis and apoptosis, and the generation of reactive oxygen species (ROS) compared to dgVDBP. Methods: Flow cytometry was used to measure superoxide anion radical (O2*−) levels and macrophage activity in the presence of VitD-dgVDBP or dgVDBP. VitD-dgVDBP was incubated with normal human lymphocytes (nPBMCs), and several clusters of determination (CDs) were estimated. dgVDBP and VitD-dgVDBP apoptosis was estimated on malignant prostatic cells. Results: The macrophage activity was 2.8-fold higher using VitD-dgVDBP (19.8·106 counts) compared to dgVDBP (7.0·106 counts), but O2*− production was 1.8-fold lower in favor of VitD-dgVDBP (355·103 counts) compared to dgVDBP (630·106 counts). The calculated ratio of the radical/macrophage activity was 5-fold lower compared to that of dgVDBP. Only VitD-dgVDBP activated caspase-3 (8%), caspase-9 (13%), and cytochrome-C (11%) on prostatic cancer cells. PE-Cy7-labeled VitD-dgVDBP was found to bind to cytotoxic suppressor cells, monocytes/macrophages, dendritic and natural killer cells (CD8+), and helper cells (CD4+). After 12 h of co-incubation of nPBMCs with VitD-dgVDBP, significant activation and expression were measured for CD16++/CD16 (0.6 ± 0.1% vs. 0.4 ± 0.1%, p < 0.05), CD45k+ (96.0 ± 6.0% vs. 84.7 ± 9.5%, p < 0.05), CD85k+ (24.3 ± 13.2% vs. 3.8 ± 3.2%, p < 0.05), and CD85k+/CD123+ (46.8 ± 8.1% vs. 3.5 ± 3.7%, p < 0.001) compared to the control experiment. No significant difference was found using CD3+, CD4+, CD8+, CD4/CD8, CD4/CD8, CD16+, CD16++, CD14+, or CD123+. A significant decline in CD14+/CD16+ was obtained in the presence of VitD-dgVDBP (0.7 ± 0.2% vs. 3.1 ± 1.7%; p < 0.01). Conclusion: The newly developed water-soluble VitD3 form VitD-dgVDBP affected cytotoxic suppressor cells by activating the low radical-dependent CD16 pathway and seemed to induce apoptosis in malignant prostatic cells.

Indexed as

calcidiol (calcifediol, 25OHD, 25-hydroxy-vitamin D)calcitriol (1α,25-dihydroxycholecalciferol, 1,25(OH)2D, or vitamin D hormone)deglycosylated vitamin D binding protein (dgVDBPGcMaf)human peripheral blood mononuclear cell (PBMC)lipopolysaccharide (LPO)reactive oxygen radicals (ROS)vitamin D3 complexed to deglycosylated vitamin D binding protein (VitD-dgVDBP)vitamin D3 (VitD3, cholecalciferol)vitamin D binding protein (VDBP)

Identifiers

PMID35892685
PMCPMC9331816

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Registered trials

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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.