ArticleScientific reports2016
A novel podocyte gene, semaphorin 3G, protects glomerular podocyte from lipopolysaccharide-induced inflammation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Nephrotic syndrome induces the upregulation of cell proliferation-related genes in tubular cells in mice.Clinical and experimental nephrology · 2025Article
- Article
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Mechanism of action ofHeliyon · 2024Article
- Article
- Decoding the Intercellular Cross-Talking Between Immune Cells and Renal Innate Cells in Diabetic Kidney Disease by Bioinformatics.Journal of inflammation research · 2023Article
- Knockdown of SEMA7A alleviates MPPImmunity, inflammation and disease · 2023Article
- Semaphorin 3G exacerbates joint inflammation through the accumulation and proliferation of macrophages in the synovium.Arthritis research & therapy · 2022Article
- Single-Cell Transcriptomics Reveal Disrupted Kidney Filter Cell-Cell Interactions after Early and Selective Podocyte Injury.The American journal of pathology · 2022Article
- Axon guidance molecules in immunometabolic diseases.Inflammation and regeneration · 2022Review
- A novel podocyte protein, R3h domain containing-like, inhibits TGF-β-induced p38 MAPK and regulates the structure of podocytes and glomerular basement membrane.Journal of molecular medicine (Berlin, Germany) · 2021Article
- The Role of Semaphorins in Metabolic Disorders.International journal of molecular sciences · 2020Review
- The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Article
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16 authors.
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Abstract
Kidney diseases including diabetic nephropathy have become huge medical problems, although its precise mechanisms are still far from understood. In order to increase our knowledge about the patho-physiology of kidney, we have previously identified >300 kidney glomerulus-enriched transcripts through large-scale sequencing and microarray profiling of the mouse glomerular transcriptome. One of the glomerulus-specific transcripts identified was semaphorin 3G (Sema3G) which belongs to the semaphorin family. The aim of this study was to analyze both the in vivo and in vitro functions of Sema3G in the kidney. Sema3G was expressed in glomerular podocytes. Although Sema3G knockout mice did not show obvious glomerular defects, ultrastructural analyses revealed partially aberrant podocyte foot processes structures. When these mice were injected with lipopolysaccharide to induce acute inflammation or streptozotocin to induce diabetes, the lack of Sema3G resulted in increased albuminuria. The lack of Sema3G in podocytes also enhanced the expression of inflammatory cytokines including chemokine ligand 2 and interleukin 6. On the other hand, the presence of Sema3G attenuated their expression through the inhibition of lipopolysaccharide-induced Toll like receptor 4 signaling. Taken together, our results surmise that the Sema3G protein is secreted by podocytes and protects podocytes from inflammatory kidney diseases and diabetic nephropathy.
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