title: Plasma soluble fas and soluble fas ligand in chronic glomerulonephritis.
abstract: It has been reported that glomerular cells with apoptosis and positive Fas immunoreactivity are seen in proliferative glomerulonephritis (PGN). Fas induces apoptosis when it binds to Fas ligand (Fas-L) or soluble Fas-L (sFas-L). However, soluble Fas (sFas) blocks apoptosis by inhibiting binding between Fas and Fas-L or sFas-L. That is, Fas, Fas-L, and sFas-L are inducers of apoptosis, but sFas is an inhibitor of apoptosis. We studied the relationship between the plasma levels of sFas and sFas-L in 32 patients with various types of adult chronic glomerulonephritis. Patients with serum creatinine levels >1.5 mg/dl (132.6 micromol/l) were excluded. The plasma levels of sFas-L were within the normal limits in all patients. The plasma levels of sFas in the patients with minimal-change (n = 8) and membranous nephropathy (n = 7) were similar to the age- and sex-matched controls. However, the plasma sFas levels were significantly elevated in patients with mesangial PGN (n = 10) and membranoproliferative glomerulonephritis (n = 7)(3. 4 +/- 0.9 and 3.9 +/- 1.5 ng/ml, respectively) as compared with the age- and sex-matched controls (controls: 2.1 +/- 0.4 and 2.2 +/- 0.6 ng/ml, respectively). In PGN, according to increase of histological grade and decrease of creatinine clearance, the number of TUNEL-positive cells in glomeruli is decreased in spite of an increase of the Fas positivity, and plasma sFas is increased. The degree of proliferative change is determined by the balance between proliferation and apoptosis and/or necrosis. Therefore, increased plasma sFas in PGN may inhibit apoptosis in glomeruli and may be one of the progressing factors in PGN. Thus, we conclude that an increase in plasma sFas levels is important to the protection of apoptosis in PGN.
authors.affiliation: 2nd Department of Internal Medicine, Gifu University School of Medicine, Gifu Prefectural Hospital, Gifu, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: K
authors.initials: K
authors.lastname: Asano
authors.forename: S
authors.initials: S
authors.lastname: Minatoguchi
authors.forename: J
authors.initials: J
authors.lastname: Hiraoka
authors.forename: K
authors.initials: K
authors.lastname: Fujisawa
authors.forename: K
authors.initials: K
authors.lastname: Nishigaki
authors.forename: N
authors.initials: N
authors.lastname: Yasuda
authors.forename: H
authors.initials: H
authors.lastname: Kumada
authors.forename: M
authors.initials: M
authors.lastname: Takemura
authors.forename: H
authors.initials: H
authors.lastname: Ohashi
authors.forename: M
authors.initials: M
authors.lastname: Seishima
authors.forename: T
authors.initials: T
authors.lastname: Fujiwara
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000276:immunology; D001706:Biopsy; D016022:Case-Control Studies; D002908:Chronic Disease; D003404:Creatinine / Q000493:pharmacokinetics; D053222:Fas Ligand Protein; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D020287:In Situ Nick-End Labeling; D015850:Interleukin-6 / Q000378:metabolism; D008024:Ligands; D016014:Linear Models; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D012995:Solubility; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019014:fas Receptor / Q000097:blood* / Q000652:urine
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D015850:Interleukin-6; D008024:Ligands; D008562:Membrane Glycoproteins; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D003404:Creatinine