ArticleMolecular immunology2006
Selective inhibition of the C5a chemotactic cofactor function of the vitamin D binding protein by 1,25(OH)2 vitamin D3.
Article in Molecular immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Integration of protein context improves protein-based COVID-19 patient stratification.Clinical proteomics · 2022Article
- Free vitamin DEuropean journal of neurology · 2022Article
- The Isoform GC1f of the Vitamin D Binding Protein Is Associated with Bronchiectasis Severity.Biomedicines · 2021Article
- 1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway.Journal of bone and mineral metabolism · 2019Article
- The Vitamin D Binding Protein and Inflammatory Injury: A Mediator or Sentinel of Tissue Damage?Frontiers in endocrinology · 2019Review
- Vitamin D Binding Protein, Total and Free Vitamin D Levels in Different Physiological and Pathophysiological Conditions.Frontiers in endocrinology · 2019Review
- Neutrophil recruitment to the lung in both C5a- and CXCL1-induced alveolitis is impaired in vitamin D-binding protein-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Vitamin D-binding protein in cerebrospinal fluid is associated with multiple sclerosis progression.Molecular neurobiology · 2013Article
- Corticosteroid therapy, vitamin D status, and inflammatory cytokine profile in the HIV-tuberculosis immune reconstitution inflammatory syndrome.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2012Article
- Proteomics comparison of cerebrospinal fluid of relapsing remitting and primary progressive multiple sclerosis.PloS one · 2010Article
- Identification of two distinct cell binding sequences in the vitamin D binding protein.Biochimica et biophysica acta · 2010Article
- Inhibitor of NF-kappa B kinases alpha and beta are both essential for high mobility group box 1-mediated chemotaxis [corrected].Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Fatty acid-binding site environments of serum vitamin D-binding protein and albumin are different.Bioorganic chemistry · 2008Article
- Cross-talk among structural domains of human DBP upon binding 25-hydroxyvitamin D.Biochemical and biophysical research communications · 2008Article
- Common variants of the vitamin D binding protein gene and adverse health outcomes.Critical reviews in clinical laboratory sciencesReview
- Hypovitaminosis D in the elderly: from bone to brain.The journal of nutrition, health & agingReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Vitamin D binding protein (DBP) is a multifunctional plasma protein that can significantly enhance the chemotactic response to complement fragment C5a. The chemotactic cofactor function of DBP requires cell surface binding in order to mediate this process. The goal of this study was to investigate the effect of ligating DBP with its two primary physiological ligands, Vitamin D and G-actin, on both binding to neutrophils and the ability to enhance chemotaxis to C5a. There was no difference in neutrophil binding between of the holo (bound) forms versus the apo (unbound) form of radioiodinated DBP, indicating that the cell binding region of DBP is likely distinct from the Vitamin D sterol and G-actin binding sites. Likewise, G-actin, 25(OH)D3, and G-actin plus 25(OH)D3 bound to DBP did not alter its capacity to enhance chemotaxis toward C5a. However, the active form of Vitamin D (1,25(OH)2D3) completely eliminated the chemotactic cofactor function of DBP. Dose-response curves demonstrated that as little as 1pM 1,25(OH)2D3 significantly inhibited chemotaxis enhancement. Moreover, at physiological concentrations 1,25(OH)2D3 needs to be bound to DBP to mediate the inhibitory effect. Neutrophil chemotaxis to optimal concentrations of C5a, formyl peptide, CXCL8 or leukotriene B4 was not altered by 1,25(OH)2D3, indicating that the active vitamin does not have a global inhibitory effect on neutrophil chemotaxis. Finally, inhibition of cell surface alkaline phosphatase (AP) with sodium orthovanadate completely reversed the inhibitory effect of 1,25(OH)2D3. These results indicate that the cell binding and co-chemotactic functions of DBP are not altered when the protein binds G-actin and/or Vitamin D. Furthermore, the co-chemotactic signal from DBP can be eliminated or counteracted by 1,25(OH)2D3.
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