Submitted by: sdemir   Date: 2018-12-25 08:33
The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection

J Biomed Biotechnol. 2012;2012:417675. doi: 10.1155/2012/417675. Epub 2012 Oct 14.

Takashi Oda,1 Nobuyuki Yoshizawa,2 Kazuo Yamakami,3 Yutaka Sakurai,3 Hanako Takechi,1
Kojiro Yamamoto,1 Naoki Oshima,1 and Hiroo Kumagai1
1Department of Nephrology, National Defense Medical College, 3-2 Namiki, Tokorozawa-shi, Saitama 359-8513, Japan
2Hemodialysis Unit, Himawari Clinic, Tokyo 196-0015, Japan
3Department of Preventive Medicine and Public Health, National Defense Medical College, Saiatama 359-8513, Japan

It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexes in situ and/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen nephritis-associated plasmin receptor (NAPlr). Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in essentially all patients with early-phase APSGN. Furthermore, glomerular plasmin activity was detected by in situ zymography in the distribution almost identical to NAPlr deposition in renal biopsy tissues of APSGN patients. These data suggest that NAPlr has a direct, nonimmunologic function as a plasmin receptor and may contribute to the pathogenesis of APSGN by maintaining plasmin activity.

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