Cleavage of the Fifth Component of Human Complement and Release of a Split Product with C5a-like Activity by Crystalline Silica through Free Radical Generation and Kallikrein Activation

Governa, M; Fenoglio, Ivana; Amati, Monica; Valentino, Matteo; Bolognini, Lucia; Coloccini, Sabrina; Volpe, Anna; Carmignani, M.; Fubini, Bice

doi:10.1006/taap.2002.9351

Cited by 20 publications

(9 citation statements)

References 37 publications

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“…The feces of the house dust mite Dermatophagoides farinae contain a protease, DerP1, which can generate active complement peptides from C3 and C5 (Maruo et al, 1997). Asbestos and silica can also cause the cleavage of C5 (Governa et al, 2000(Governa et al, , 2002(Governa et al, , 2005. More recently, cross-talk between the complement and the coagulation cascades has been demonstrated to result in the robust generation of C3a and C5a, through the actions of factors Xa/XIa, plasmin, and thrombin (Amara et al, 2010).…”

Section: C3a and C5a Generation Outside The Complement Cascadementioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors

Klos

Wende²,

Wareham³

et al. 2013

Pharmacol Rev

232

245

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Section: C3a and C5a Generation Outside The Complement Cascadementioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors

Klos

Wende²,

Wareham³

et al. 2013

Pharmacol Rev

232

245

View full text Add to dashboard Cite

“…Iron presence in RCA, due to environmental contamination, was found at the chrysotile fiber surface and mostly in the ferrous phase (Governa et al, 2002). Ferrous ions via a Fenton-type reaction catalyse the production of hydroxyl radicals that compromise exposed biological systems.…”

Section: Discussionmentioning

confidence: 99%

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

et al. 2015

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“…This suggested that the complement system was activated in TCE-induced renal injury. Evidence suggests the complement system is closely linked to the KKS (Governa et al 2002). During activation of innate immunity, PK in local tissue plays a promoting role through activation of C3 (Oikonomopoulou et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice

Wang

Zhang

et al. 2016

Journal of Immunotoxicology

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Trichloroethylene (TCE) is a major environmental pollutant. An immunological response is a newlyrecognized mechanism for TCE-induced kidney damage. However, the role of the plasma kallikreinkinin system (KKS) in immune-mediated kidney injury has never been examined. This study aimed to explore the role of the key components of the KKS, i.e. plasma kallikrein (PK), bradykinin (BK) and its receptors B1R and B2R, in TCE-induced kidney injury. A mouse model of skin sensitization was used to explore the mechanism of injury with or without a PK inhibitor PKSI. Kidney function was evaluated by measuring blood urea nitrogen (BUN) and creatinine (Cr) in conjunction with histopathologic characterization. Plasma BK was determined by ELISA; Renal C5b-9 membrane attack complex was evaluated by immunohistochemistry. Expression of BK and PK in the kidney was detected by immunoFuorescence. mRNA and protein levels of B1R and B2R were assessed by real-time qPCR and Western blot. As expected, numerous inflammatory cell inEltration and tubular epithelial cell vacuolar degeneration were observed in TCE-sensitized mice. Moreover, serum BUN and Cr and plasma BK were increased. In addition, deposition of BK, PK and C5b-9 were observed and B1R and B2R mRNA and proteins levels were up-regulated. Pre-treatment with PKSI, a highly selective inhibitor of PK, alleviated TCE-induced renal damage. In addition, PKSI attenuated TCEinduced up-regulation of BK, PK and its receptors and C5b-9. These results provided the first evidence that activation of the KKS contributed to immune-mediated renal injury induced by TCE and also helped to identify the KKS as a potential therapeutic target for mitigating chemical sensitization-induced renal damage.ARTICLE HISTORY

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Cleavage of the Fifth Component of Human Complement and Release of a Split Product with C5a-like Activity by Crystalline Silica through Free Radical Generation and Kallikrein Activation

Cited by 20 publications

References 37 publications

International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors

International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice

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