ArticleInflammation2022
Interleukin-6 Downregulates the Expression of Vascular Endothelial-Cadherin and Increases Permeability in Renal Glomerular Endothelial Cells via the Trans-Signaling Pathway.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Sarsasapogenin Preserves Podocyte Integrity and Attenuates Renal Injury in Experimental IgA Nephropathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Modeling the synovium on a chip for studying the interactions between lymphatic vasculature and synoviocytes in rheumatoid arthritis.Biofabrication · 2026Article
- Breast Cancer-Associated Venous Thromboembolism: Risk Factors, Mechanisms, and Clinical Management.Cancers · 2026Review
- NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation.Frontiers in cardiovascular medicine · 2026Article
- SAPHO syndrome with membranous nephropathy and analgesic-induced nephropathy: a case report.Frontiers in immunology · 2026Article
- Protective Effects of Luteolin onAntibiotics (Basel, Switzerland) · 2025Article
- Logic-based modeling of inflammatory macrophage cross talk with glomerular endothelial cells in diabetic kidney disease.American journal of physiology. Renal physiology · 2025Article
- Inflammation-associated molecules in the glomerular-endothelium in mild IgA-nephropathy patients identified by single-cell and spatial transcriptome.Communications biology · 2025Article
- ARNT-dependent HIF-2α signaling protects cardiac microvascular barrier integrity and heart function post-myocardial infarction.Communications biology · 2025Article
- Single-Cell Analysis of Endothelial Cell Injury in IgA Nephropathy.Immunity, inflammation and disease · 2025Article
- CAR T-Cell Therapy in Cancer: Balancing Efficacy with Cardiac Toxicity Concerns.Journal of cancer science and clinical therapeutics · 2025Article
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- Endothelial Cell Dysfunction and Increased Cardiovascular Risk in Patients With Chronic Kidney Disease.Circulation research · 2023Review
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- Loss of filamentous actin, tight junction protein expression, and paracellular barrier integrity in frataxin-deficient human brain microvascular endothelial cells-implications for blood-brain barrier physiology in Friedreich's ataxia.Frontiers in molecular biosciences · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The pathogenesis of IgA nephropathy (IgAN) is still unknown, but reportedly, interleukin 6 (IL-6) is involved in this process. However, its role in damaging glomerular endothelial cells is still unclear. Therefore, in this study, to clarify the mechanism of the pathogenesis of IgAN, we investigated the effect of IL-6 on the permeability of glomerular endothelial cells. A rat model of IgAN was established, and the animals divided into two groups, namely, the normal and IgAN groups. Glomerular endothelial cell injury was evaluated via electron microscopy. Furthermore, IL-6-induced changes in the permeability of human renal glomerular endothelial cells (HRGECs) were measured via trans-endothelial resistance (TEER) measurements and fluorescein isothiocyanate-dextran fluorescence. Furthermore, vascular endothelial-cadherin (VE-cadherin) was overexpressed to clarify the effect of IL-6 on HRGEC permeability, and to determine the pathway by which it acts. The classical signaling pathway was blocked by silencing IL-6R and the trans-signaling pathway was blocked by sgp30Fc. In IgAN rats, electron microscopy showed glomerular endothelial cell damage and western blotting revealed a significant increase in IL-6 expression, while VE-cadherin expression decreased significantly in the renal tissues. IL-6/IL-6R stimulation also significantly increased the permeability of HRGECs (p < 0.05). This effect was significantly reduced by VE-cadherin overexpression (p < 0.01). After IL-6R was silenced, IL-6/IL-6R still significantly reduced VE-cadherin expression and sgp30Fc blocked the trans-signaling pathway as well as the upregulation of IL-6/IL-6R-induced VE-cadherin expression. This suggests that IL-6 mainly acts via the trans-signaling pathway. IL-6 increased the permeability of HRGECs by decreasing the expression of VE-cadherin via the trans-signaling pathway.
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