ArticleBiochimica et biophysica acta2014
Signaling components of the 1α,25(OH)2D3-dependent Pdia3 receptor complex are required for Wnt5a calcium-dependent signaling.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Combined Effects of Vitamin D3 and Extracorporeal Shockwave Therapy on Osteoblast Differentiation via F-actin mediated Pdia3 Membrane Localization.International journal of medical sciences · 2026Article
- 24R,25(OH)International journal of cancer · 2026Article
- Review
- Nongenomic Activities of Vitamin D.Nutrients · 2022Review
- The human WNT5A isoforms display similar patterns of expression but distinct and overlapping activities in normal human osteoblasts.Journal of cellular biochemistry · 2021Article
- A hierarchical regulatory network analysis of the vitamin D induced transcriptome reveals novel regulators and complete VDR dependency in monocytes.Scientific reports · 2021Article
- The Relative Expression of ERα Isoforms ERα66 and ERα36 Controls the Cellular Response to 24R,25-Dihydroxyvitamin D3 in Breast Cancer.Molecular cancer research : MCR · 2021Article
- Article
- Loss of Estrogen Receptors is Associated with Increased Tumor Aggression in Laryngeal Squamous Cell Carcinoma.Scientific reports · 2020Article
- Lef1 regulates caveolin expression and caveolin dependent endocytosis, a process necessary for Wnt5a/Ror2 signaling during Xenopus gastrulation.Scientific reports · 2019Article
- Caveolin-1 down-regulation is required for Wnt5a-Frizzled 2 signalling in Ha-RasJournal of cellular and molecular medicine · 2018Article
- Wnt5a induces catabolic signaling and matrix metalloproteinase production in human articular chondrocytes.Osteoarthritis and cartilage · 2017Article
- Extracorporeal Shockwave Therapy Enhances Expression of Pdia-3 Which Is a Key Factor of the 1α,25-Dihydroxyvitamin D 3 Rapid Membrane Signaling Pathway in Treatment of Early Osteoarthritis of the Knee.International journal of medical sciences · 2017Article
- Analysis of the interaction of calcitriol with the disulfide isomerase ERp57.Scientific reports · 2016Article
- Implant Surface Design Regulates Mesenchymal Stem Cell Differentiation and Maturation.Advances in dental research · 2016Review
- Integrative network-based analysis of mRNA and microRNA expression in 1,25-dihydroxyvitamin D3-treated cancer cells.Genes & nutrition · 2015Article
- Membrane-mediated actions of 1,25-dihydroxy vitamin D3: a review of the roles of phospholipase A2 activating protein and Ca(2+)/calmodulin-dependent protein kinase II.The Journal of steroid biochemistry and molecular biology · 2015Review
- Impaired bone formation in Pdia3 deficient mice.PloS one · 2014Article
- Possible role of vitamin D3 on the adipocyte/fibroblast trans-differentiation mediated by pancreas cancerCurrent health sciences journalArticle
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Wnt5a and 1α,25(OH)2D3 are important regulators of endochondral ossification. In osteoblasts and growth plate chondrocytes, 1α,25(OH)2D3 initiates rapid effects via its membrane-associated receptor protein disulfide isomerase A3 (Pdia3) in caveolae, activating phospholipase A2 (PLA2)-activating protein (PLAA), calcium/calmodulin-dependent protein kinase II (CaMKII), and PLA2, resulting in protein kinase C (PKC) activation. Wnt5a initiates its calcium-dependent effects via intracellular calcium release, activating PKC and CaMKII. We investigated the requirement for components of the Pdia3 receptor complex in Wnt5a calcium-dependent signaling. We determined that Wnt5a signals through a CaMKII/PLA2/PGE2/PKC cascade. Silencing or blocking Pdia3, PLAA, or vitamin D receptor (VDR), and inhibition of calmodulin (CaM), CaMKII, or PLA2 inhibited Wnt5a-induced PKC activity. Wnt5a activated PKC in caveolin-1-silenced cells, but methyl-beta-cyclodextrin reduced its stimulatory effect. 1α,25(OH)2D3 reduced stimulatory effects of Wnt5a on PKC in a dose-dependent manner. In contrast, Wnt5a had a biphasic effect on 1α,25(OH)2D3-stimulated PKC activation; 50ng/ml Wnt5a caused a 2-fold increase in 1α,25(OH)2D3-stimulated PKC but higher Wnt5a concentrations reduced 1α,25(OH)2D3-stimulated PKC activation. Western blots showed that Wnt receptors Frizzled2 (FZD2) and Frizzled5 (FZD5), and receptor tyrosine kinase-like orphan receptor 2 (ROR2) were localized to caveolae. Blocking ROR2, but not FZD2 or FZD5, abolished the stimulatory effects of 1α,25(OH)2D3 on PKC and CaMKII. 1α,25(OH)2D3 membrane receptor complex components (Pdia3, PLAA, caveolin-1, CaM) interacted with Wnt5a receptors/co-receptors (ROR2, FZD2, FZD5) in immunoprecipitation studies, interactions that changed with either 1α,25(OH)2D3 or Wnt5a treatment. This study demonstrates that 1α,25(OH)2D3 and Wnt5a mediate their effects via similar receptor components and suggests that these pathways may interact.
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