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A novel podocyte gene, semaphorin 3G, protects glomerular podocyte from lipopolysaccharide-induced inflammation
Chiba Univ, Grad Sch Med, Dept Clin Cell Biol & Med, Chiba, Japan.;Chiba Univ Hosp, Div Diabet Metab & Endocrinol, Chiba, Japan..
Chiba Univ, Grad Sch Med, Dept Clin Cell Biol & Med, Chiba, Japan.;Chiba Univ Hosp, Div Diabet Metab & Endocrinol, Chiba, Japan..
Kyorin Univ, Sch Med, Dept Anat, Mitaka, Tokyo 181, Japan..
Chiba Univ, Grad Sch Med, Dept Clin Cell Biol & Med, Chiba, Japan.;Chiba Univ Hosp, Div Diabet Metab & Endocrinol, Chiba, Japan..
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2016 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 6, 25955Article in journal (Refereed) Published
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Abstract [en]

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 pathophysiology 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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2016. Vol. 6, 25955
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Cancer and Oncology
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URN: urn:nbn:se:uu:diva-297781DOI: 10.1038/srep25955ISI: 000375903600001PubMedID: 27180624OAI: oai:DiVA.org:uu-297781DiVA: diva2:943630
Available from: 2016-06-28 Created: 2016-06-28 Last updated: 2017-11-28Bibliographically approved

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Betsholtz, Christer

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