Human complement protein D catabolism by the rat kidney.

Sanders, Paul W.; Volanakis, John E.; Rostand, Stephen G.; Galla, John H.

doi:10.1172/jci112434

Cited by 23 publications

(15 citation statements)

References 34 publications

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“…The preparation for micropuncture was similar to the method described previously (5). Male Sprague-Dawley rats (Charles River Breeding Laboratories, Inc., Wilmington, MA, or Taconic Farms, Inc., Germantown, NY), which weighed 220-325 g (285±2 g) and were maintained on standard rat chow (Agway/Prolab 1000, Syracuse, NY) and tap water ad lib., were anesthetized with ethyl, 1-methylpropylthiobarbiturate (Inactin; BYK Gulden, FRG), 100 mg/kg body weight (BW) i.p.…”

Section: Methodsmentioning

confidence: 99%

Differential nephrotoxicity of low molecular weight proteins including Bence Jones proteins in the perfused rat nephron in vivo.

Sanders¹,

Herrera²,

A³

et al. 1988

J. Clin. Invest.

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To investigate the pathogenetic mechanisms of tubule nephrotoxicity of low molecular weight proteins (LMWP), proximal tubules (PT) of rats were perfused in vivo with artificial tubule fluid (ATF) containing one of five LMWPs: three human Bence Jones proteins (BJP), f-lactoglobulin (BLG), and rabbit myoglobin (MYG). Volume (J4), chloride (Jce) and glucose (JG) fluxes in these perfused PTs were compared with those determined using ATF alone. In separate experiments, perfused nephrons were examined with electron and immunoelectron microscopy. After exposure to IHJP1 or BLG, Jv, Jc0, and JG were less (P < 0.05) than corresponding control fluxes. Cell damage of these perfused PTs, along with cellular debris in the distal tubules, was prominent. The PT lysosomes often appeared atypical and contained crystals. In contrast, perfusion with BJP2, BJP3, or MYG did not alter Jv, Jcj, or JG. These findings were corroborated by the normal ultrastructure of these PTs despite immunohistochemical evidence of endocytosis of the BJPs. Isoelectric point, molecular form, and isotype were not factors associated with PT damage. In addition, proteins with pI < 7.4 precipitated in the distal nephron, forming acellular casts.

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Section: Methodsmentioning

confidence: 99%

Differential nephrotoxicity of low molecular weight proteins including Bence Jones proteins in the perfused rat nephron in vivo.

Sanders¹,

Herrera²,

A³

et al. 1988

J. Clin. Invest.

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“…In addition to inhibiting the alternative pathway, an anti-FD antibody indirectly also blocks classical and mannose-binding lectin pathways, as amplification of these pathways depends on alternative pathway convertase activation (7,8). The low concentration of FD in blood is maintained by an extremely rapid catabolic rate (6,9,10). Systemic treatment with blocking anti-FD antibodies would require very high dosing to overcome the high turnover rate (11).…”

mentioning

confidence: 99%

Inhibiting Alternative Pathway Complement Activation by Targeting the Factor D Exosite

Katschke¹,

Wu²,

Ganesan³

et al. 2012

Journal of Biological Chemistry

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Background: Anti-factor D antibody blocks a rate-limiting step in the alternative complement pathway. Results: The structure of anti-factor D in complex with factor D provides the molecular basis of complement inhibition. Conclusion: Anti-factor D binds to the factor D exosite and inhibits alternative pathway complement activation. Significance: Targeting the exosite on proteases could have great potential for antibody therapies.

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“…Description of the anesthesia and surgical preparation of the rats used for in vivo microperfusion of the LS has been standardized in our laboratory and reported in detail (6,8,19). Briefly, male Sprague-Dawley rats (Charles River Breeding Laboratories, Inc., Wilmington, MA, and National Cancer Institute, Frederick, MD), which weighed between 160 and 310 g (mean, 230±7 g) and were maintained on standard rat chow (Prolab 1000; Agway Inc., Syracuse, NY) and tap water ad lib., were anesthetized with ethyl, 1-methylpropylthiobarbiturate (Inactin; BYK Gulden, FRG), 100 mg/kg body weight (BW), intraperitoneally.…”

mentioning

confidence: 99%

Mechanisms of intranephronal proteinaceous cast formation by low molecular weight proteins.

Sanders¹,

Booker²,

Bishop³

et al. 1990

J. Clin. Invest.

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118

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Proteinaceous cast formation in the distal nephron of the kidney from low molecular weight proteinuria is a significant, but poorly characterized, cause of renal failure. To study this phenomenon, we: (a) microperfused the loop segment (LS) of rats in vivo with artificial tubule fluid (ATF) containing four different low molecular weight proteins, 0.01-50 mg/ml, to detect alterations in LS function, and (b) examined the interaction between several proteins and Tamm

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Human complement protein D catabolism by the rat kidney.

Cited by 23 publications

References 34 publications

Differential nephrotoxicity of low molecular weight proteins including Bence Jones proteins in the perfused rat nephron in vivo.

Differential nephrotoxicity of low molecular weight proteins including Bence Jones proteins in the perfused rat nephron in vivo.

Inhibiting Alternative Pathway Complement Activation by Targeting the Factor D Exosite

Mechanisms of intranephronal proteinaceous cast formation by low molecular weight proteins.

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