Plasma Soluble Fas and Soluble Fas Ligand in ChronicGlomerulo nephritis

Sano, Hirotake; Asano, Kiyoji; Minatoguchi, Shinya; Hiraoka, Jitsuko; Fujisawa, Koh; Nishigaki, Kazuhiko; Yasuda, Norio; Kumada, Hirokazu; Takemura, Masao; Ohashi, Hiroshige; Seishima, Mitsuru; Fujiwara, Takako; Fujiwara, Hisayoshi

doi:10.1159/000045159

Cited by 18 publications

(22 citation statements)

References 22 publications

(39 reference statements)

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“…As previously reported, apoptotic cells were observed during the progression of glomerulosclerosis in the remnant-kidney model [3], in glomerulonephritis [11], and in mesangial cell proliferative lesions in severe glomerular lesions from IgA nephropathy [19]. Overexpression of Fas in the glomeruli may be related to an increase in sFas [11, 19]. However, in the present study, we could demonstrate no correlation between them, and the expression of Fas antigen on MNCs presented concomitantly with the elevation in sFas.…”

Section: Discussionsupporting

confidence: 56%

“…However, no significant correlation was obtained between the number of apoptotic cells and the percentage of Fas-positive MNCs/sFas levels. As previously reported, apoptotic cells were observed during the progression of glomerulosclerosis in the remnant-kidney model [3], in glomerulonephritis [11], and in mesangial cell proliferative lesions in severe glomerular lesions from IgA nephropathy [19]. Overexpression of Fas in the glomeruli may be related to an increase in sFas [11, 19].…”

Section: Discussionmentioning

confidence: 55%

“…High serum levels of sFas and sFasL have been reported in patients with autoimmune diseases, such as SLE, rheumatoid arthritis, UCTD, and vasculitis [10]. The same items were analyzed in patients with chronic glomerulonephritis, and it was concluded that increased plasma sFas in proliferative glomerulonephritis may inhibit apoptosis in the glomeruli and may be a disease-progessing factor [11]. …”

Section: Introductionmentioning

confidence: 99%

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Fas-Fas Ligand System in the Peripheral Blood of Patients with Renal Diseases

Sato

Konuma²,

Yanagisawa³

et al. 2000

Nephron

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To clarify the role of the Fas-Fas ligand (FasL) system in the peripheral blood from patients with various renal diseases, the Fas and FasL expression on mononuclear cells (MNCs) and serum levels of soluble Fas (sFas) and soluble FasL were investigated. Patients were selected from those with various types of glomerular diseases showing various degrees of renal function. Fas expression on MNCs was analyzed by a FACScan, sFas and soluble FasL were measured with an ELISA kit, and FasL expression on MNCs was counted using a FACScan after a bioassay. Fas-positive MNCs and sFas increased with statistical significance concomitantly with deterioration in renal function. Moreover, there was a significant correlation between them. sFas- and FasL-positive MNCs were significantly correlated with proteinuria. However, the Fas expression percentage on MNCs and/or serum levels of sFas did not correlate with the number of TUNEL-positive cells in the glomeruli. Also, there was no disease specificity in the activation of Fas. These results indicate that Fas expression on MNCs is activated in accordance with the deterioration in renal function without disease specificity, corresponding to the elevation of serum sFas levels to protect against Fas-mediated apoptosis.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

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Fas-Fas Ligand System in the Peripheral Blood of Patients with Renal Diseases

Sato

Konuma²,

Yanagisawa³

et al. 2000

Nephron

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“…It decreases the number of TUNNEL-positive cells in the glomeruli, promoting its progressive injury in the mechanism of apoptosis-proliferation deregulation (36, 37). The significantly increased pre-treatment values for urinary excretion of sFas in Non-Responders with proliferative GN seem to support this.…”

Section: Discussionmentioning

confidence: 99%

S-Fas Urinary Excretion Helps to Predict the Immunosuppressive Treatment Outcomes in Patients with Proliferative Primary Glomerulonephritis

Zwiech

2013

J Korean Med Sci

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Deregulation of soluble apoptosis stimulating fragment (sFas) plays an important role in glomerulonephritis (GN). The study assed the influence of immunosuppressive treatment on serum and urine sFas in patients with proliferative (PGN) and non-proliferative (NPGN) GN, and evaluated the potential of sFas measurements in predicting outcomes. Eighty-four patients with GN (45 males and 39 females) were included. Serum concentration (ng/mL) and urinary excretion (ng/mg of urinary creatinine) of sFas were measured before and after the treatment. After 12 months of therapy with steroids and cyclophosphamide, patients were divided into two subgroups according to the treatment results: Responders (R) and Non-Responders (NR). The sFas urinary excretion was reduced after treatment in both PGN and NPGN (from 17.12 ± 15 to 5.3 ± 4.2, P = 0.008 and from 10.11 ± 6.1 to 3.4 ± 3.0, P = 0.039; respectively) whereas the sFas serum concentration remained unchanged. In PGN, pre-treatment urinary sFas concentration was significantly lower in the Responders than in Non-Responders (2.3 ± 3.1 vs 19.4 ± 14.1, P = 0.003), and was lower still than in both R (P = 0.044) and NR (P = 0.042) subgroups with NPGN. The immunosuppressive treatment reduced sFas urinary excretion in proliferative and non-proliferative GN and results suggest that the lower urinary sFas may be linked with favorable therapy outcomes in patients with PGN.

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“…2 Alternative splicing generates molecules with no transmembrane domain in a soluble form (sFas), which still bind to Fas-L 3 and inhibit apoptosis. 4 The intracellular domain of Fas has different binding sites for a growing number of proteins that lead to many cellular responses (Fig. 1).…”

Section: Fas and Fas-ligand Moleculesmentioning

confidence: 99%

Is the Fas/Fas-L Pathway a Promising Target for Treating Inflammatory Heart Disease?

Henriques-Pons

Oliveira

2009

Journal of Cardiovascular Pharmacology

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The elucidation of the intricate molecular network of costimulus and regulatory pathways of the immune system led to the design of molecular therapies that specifically inactivate some cellular responses and ameliorate some autoimmune and inflammatory diseases. This innovative concept opens a new class of therapies, and one of the central components that could be targeted in future molecular therapies is the Fas-based pathway. Both soluble and membrane-bound Fas and Fas-L molecules exert a wide range of proinflammatory functions through the secretion of cytokines and chemokines, cellular chemotaxis, transcriptional regulation, cellular death, and others. Accordingly, many chronic inflammatory diseases, including myocarditis, are attenuated in mice lacking either molecule. Although it is tempting to speculate that the Fas/Fas-L pathway could be targeted for in vivo myocarditis therapy, the plurality of Fas/Fas-L functions can be an obstacle, leading to important side effects. In this review, we suggest that the injection of nonagonistic antibodies raised against the Fas molecule or the inactivation of downstream Fas-1,4,5-inositol triphosphate cascade are possible targets for myocarditis treatment.

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Plasma Soluble Fas and Soluble Fas Ligand in ChronicGlomerulo nephritis

Cited by 18 publications

References 22 publications

Fas-Fas Ligand System in the Peripheral Blood of Patients with Renal Diseases

Fas-Fas Ligand System in the Peripheral Blood of Patients with Renal Diseases

S-Fas Urinary Excretion Helps to Predict the Immunosuppressive Treatment Outcomes in Patients with Proliferative Primary Glomerulonephritis

Is the Fas/Fas-L Pathway a Promising Target for Treating Inflammatory Heart Disease?

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