ArticleArthritis & rheumatology (Hoboken, N.J.)2016
Lupus Nephritis IgG Induction of Calcium/Calmodulin-Dependent Protein Kinase IV Expression in Podocytes and Alteration of Their Function.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 60 citations in OpenAlex.
- Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- The Role of Podocytes in Lupus Pathology.Current rheumatology reports · 2024Review
- Exploiting the neonatal crystallizable fragment receptor to treat kidney disease.Kidney international · 2024Review
- Immune podocytes in the immune microenvironment of lupus nephritis (Review).Molecular medicine reports · 2023Review
- The therapeutic age of the neonatal Fc receptor.Nature reviews. Immunology · 2023Review
- Anti-phospholipase A2 receptor antibodies directly induced podocyte damageRenal failure · 2022Article
- Mitochondrial impairment and repair in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2022Review
- Glycolysis in Innate Immune Cells Contributes to Autoimmunity.Frontiers in immunology · 2022Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Aberrantly glycosylated IgG elicits pathogenic signaling in podocytes and signifies lupus nephritis.JCI insight · 2021Article
- Immunometabolic Pathways and Its Therapeutic Implication in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021Review
- N-glycosylated IgG in patients with kidney transplants increases calcium/calmodulin kinase IV in podocytes and causes injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
- Cell derived extracellular matrix-rich biomimetic substrate supports podocyte proliferation, differentiation and maintenance of native phenotype.Advanced functional materials · 2020Article
- T cell metabolism: new insights in systemic lupus erythematosus pathogenesis and therapy.Nature reviews. Rheumatology · 2020Review
- Pathogenesis of lupus nephritis: RIP3 dependent necroptosis and NLRP3 inflammasome activation.Journal of autoimmunity · 2019Article
- Podocyte Injury in Lupus Nephritis.Journal of clinical medicine · 2019Review
- Vitamin D protects podocytes from autoantibodies induced injury in lupus nephritis by reducing aberrant autophagy.Arthritis research & therapy · 2019Article
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveKidney podocytes and their slit diaphragms prevent urinary protein loss. T cells from patients with systemic lupus erythematosus display increased expression of calcium/calmodulin-dependent protein kinase IV (CaMKIV). The present study was undertaken to investigate the role of CaMKIV in podocyte function in lupus nephritis (LN).
methodsWe treated kidney podocytes with IgG derived from healthy individuals or patients with LN and then analyzed gene expression using a DNA microarray. The localization of IgG in podocytes was analyzed by immunofluorescence staining, with or without silencing of neonatal Fc receptor (FcRn). In addition, we silenced CAMK4 in podocytes and analyzed the expression of selected genes. We also examined the expression of CD86 in kidney podocytes from MRL/lpr, MRL/lpr.camkiv(-/-), and MRL/MPJ mice by in situ hybridization.
resultsWe found that exposure of podocytes to IgG resulted in entry of IgG into the cytoplasm. IgG entered podocytes via the FcRn because less IgG was found in the cytoplasm of podocytes treated with FcRn small interfering RNA. DNA microarray studies of podocytes exposed to LN-derived IgG revealed up-regulation of genes related to the activation of immune cells or podocyte damage. Interestingly, CD86 expression decreased after silencing CAMK4 in podocytes. Also, in situ hybridization experiments showed that the expression of CD86 was reduced in podocytes from MRL/lpr.camkiv(-/-) mice.
conclusionLN-derived IgG enters podocytes and up-regulates CAMK4, which is followed by increased expression of genes known to be linked to podocyte damage and T cell activation. Targeted inhibition of CAMK4 in podocytes may prove to be clinically useful in patients with LN.
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