Interaction between Interferon-Stimulated Gene 56 and Melanoma Differentiation-Associated Gene 5 in Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells

2013 ◽  
Vol 37 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Tadaatsu Imaizumi ◽  
Tomomi Aizawa-Yashiro ◽  
Tomoh Matsumiya ◽  
Hidemi Yoshida ◽  
Shojiro Watanabe ◽  
...  
Keyword(s):  
Mesangial Cells ◽  
Toll Like Receptor ◽  
Human Mesangial Cells ◽  
Normal Human

scholarly journals Cellular receptors for matrix proteins in normal human kidney and human mesangial cells

1990 ◽  
Vol 38 (5) ◽  
pp. 886-895 ◽  
Author(s):  
Fernando G. Cosio ◽  
Daniel D. Sedmak ◽  
N. Stanley Nahman
Keyword(s):  
Mesangial Cells ◽  
Human Kidney ◽  
Matrix Proteins ◽  
Cellular Receptors ◽  
Human Mesangial Cells ◽  
Normal Human Kidney ◽  
Normal Human

Toll-like receptor 3 signaling contributes to the expression of a neutrophil chemoattractant, CXCL1 in human mesangial cells

2014 ◽  
Vol 19 (5) ◽  
pp. 761-770 ◽  
Author(s):  
Tadaatsu Imaizumi ◽  
Tomomi Aizawa ◽  
Chihiro Segawa ◽  
Michiko Shimada ◽  
Kazushi Tsuruga ◽  
...  
Keyword(s):  
Mesangial Cells ◽  
Toll Like Receptor ◽  
Human Mesangial Cells

scholarly journals Cylindromatosis (CYLD), a Deubiquitinase, Attenuates Inflammatory Signaling Pathways by Activating Toll-Like Receptor 3 in Human Mesangial Cells

2017 ◽  
Vol 42 (5) ◽  
pp. 942-950 ◽  
Author(s):  
Tadaatsu Imaizumi ◽  
Ryo Hayakari ◽  
Shojiro Watanabe ◽  
Tomomi Aizawa ◽  
Tomoh Matsumiya ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Mesangial Cells ◽  
Toll Like Receptor ◽  
Inflammatory Signaling ◽  
Human Mesangial Cells

scholarly journals PAPP-A in normal human mesangial cells: effect of inflammation and factors related to diabetic nephropathy

2016 ◽  
Vol 231 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Diane Donegan ◽  
Laurie K Bale ◽  
Cheryl A Conover
Keyword(s):  
Diabetic Nephropathy ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Igf System ◽  
Tnf Α ◽  
Glycation End Products ◽  
Normal Human ◽  
Matrix Production ◽  
Igf1 Receptor ◽  
Necrosis Factor

Insulin-like growth factors (IGFs) are implicated in the development of diabetic nephropathy (DN) and are shown to increase proliferation and extracellular matrix production in mesangial cells. The IGF system is complex and is composed of ligands, receptors, six binding proteins (IGF BPs) and a novel zinc metalloproteinase – pregnancy-associated plasma protein (PAPP)-A. PAPP-A increases the local bioavailability of IGF through the cleavage of IGF BP-4. Mesangial expansion is a major component of DN, and PAPP-A is shown to be increased in the glomeruli of patients with DN. Therefore, we determined the expression of PAPP-A and components of the IGF system in normal human mesangial cells (HMCs) and their regulation by factors known to be involved in DN. Under basal conditions, HMCs expressed PAPP-A, IGF1 receptor and all six IGF BPs. Interleukin (IL)-1β was the most potent stimulus for PAPP-A expression (5-fold) followed by tumor necrosis factor (TNF)-α (2.5-fold). This PAPP-A was secreted, cell associated and proteolytically active. IL1β also increased IGF BP-1expression (3-fold) with either reduction or no effect on other IGF BPs. Generally, TNF-α treatment decreased IGF BP expression. No treatment effect on PAPP-A or IGF BPs was seen with IL6, IGFs, advanced glycation end products or prolonged hyperglycemia. In addition, stimulation of HMCs with IGF1 alone or IGF1 complexed to wild-type, but not protease-resistant, IGF BP-4 led to increased [3H]-thymidine incorporation. In conclusion, these novel findings of PAPP-A and its regulation by proinflammatory cytokines, as well as the comprehensive analysis of the IGF system regulation in HMCs, suggest a mechanism by which inflammatory states such as DN can impact IGF activity in the kidney.

scholarly journals Therapeutic effects and mechanism of conditioned media from human mesenchymal stem cells on anti-GBM glomerulonephritis in WKY rats

2016 ◽  
Vol 310 (11) ◽  
pp. F1182-F1191 ◽  
Author(s):  
Ken Iseri ◽  
Masayuki Iyoda ◽  
Hirokazu Ohtaki ◽  
Kei Matsumoto ◽  
Yukihiro Wada ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Mesangial Cells ◽  
Umbilical Vein ◽  
Therapeutic Effects ◽  
Peripheral Blood Mononuclear ◽  
Human Mesangial Cells ◽  
Tnf Α ◽  
Normal Human ◽  
Umbilical Vein Endothelial Cells

Recent studies have demonstrated that conditioned media derived from mesenchymal stem cells (MSC-CM) have therapeutic effects in various experimental diseases. However, the therapeutic mechanism is not fully understood. In the present study, we investigated the therapeutic effects and mechanism of MSC-CM in experimental antiglomerular basement membrane glomerulonephritis. We administered either MSC-CM or vehicle from day 0 to day 10 after the induction of nephrotoxic serum nephritis in Wistar-Kyoto rats. In vitro, we analyzed the effects of MSC-CM on TNF-α-mediated cytokine production in cultured normal human mesangial cells, proximal tubular (HK-2) cells, human umbilical vein endothelial cells, and monocytes (THP-1 and peripheral blood mononuclear cells). Compared with vehicle treatment, MSC-CM treatment improved proteinuria and renal dysfunction. Histologically, MSC-CM-treated rats had reduced crescent formation and glomerular ED1+ macrophage infiltration and increased glomerular ED2+ macrophage infiltration. Increased serum monocyte chemoattractant protein (MCP)-1 levels were observed in MSC-CM-treated rats. Renal cortical mRNA expression levels of proinflammatory cytokines, such as TNF-α and IL-6, and of the T helper cell 1 cytokine interferon-γ were greatly decreased by MSC-CM treatment. In vitro, pretreatment with MSC-CM blocked TNF-α-mediated IL-8 release in normal human mesangial cells and HK-2 cells. TNF-α-mediated MCP-1 release was enhanced by pretreatment with MSC-CM in human umbilical vein endothelial cells and HK-2 cells and was strikingly enhanced in THP-1 cells. Stimulation of peripheral blood mononuclear cells with a combination of MCP-1 and IL-4 enhanced the expression of M2-associated genes compared with IL-4 alone. We demonstrated that MSC-CM had therapeutic effects in experimental antiglomerular basement membrane glomerulonephritis that were mediated through anti-inflammatory effects that were partly due to acceleration of M2 macrophage polarization, which might be mediated by MCP-1 enhancement.

scholarly journals Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Hiroshi Tanaka ◽  
Tadaatsu Imaizumi
Keyword(s):  
Renal Disease ◽  
Signaling Pathways ◽  
Viral Infections ◽  
Mesangial Cells ◽  
Experimental Studies ◽  
Renal Diseases ◽  
Glomerular Diseases ◽  
Human Mesangial Cells ◽  
Normal Human ◽  
Few Data

The innate and adaptive immune systems have been reported to play an important role in the pathogenesis of glomerular diseases. Since viral infections may trigger the development of inflammatory renal disease or the worsening of preexisting renal disease, recent studies have focused on the involvement of toll-like receptors (TLRs) and their signaling pathways in the inflammatory processes of glomerular cells. Viral double-stranded RNA (dsRNA) can activate not only TLR3 located within intracellular endosomes but also retinoic-acid-inducible-gene-I- (RIG-I-) like helicase receptors located within the cytosol. RIG-I and melanoma differentiation-associated gene 5 (MDA5) are members of the RNA helicase family in the cytosol, and both act as pathogen recognition receptors. The activation of TLRs and their downstream immune responses can be induced by both infectious pathogens and noninfectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. However, there are few data on the interaction between TLR3, MDA5, and RIG-I in autoimmune glomerular diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases. In the present paper, we summarize our recent findings.

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