RGD Reference Report - Early activation of bradykinin B2 receptor aggravates reactive oxygen species generation and renal damage in ischemia/reperfusion injury. - Rat Genome Database

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Early activation of bradykinin B2 receptor aggravates reactive oxygen species generation and renal damage in ischemia/reperfusion injury.

Authors: Chiang, WC  Chien, CT  Lin, WW  Lin, SL  Chen, YM  Lai, CF  Wu, KD  Chao, J  Tsai, TJ 
Citation: Chiang WC, etal., Free Radic Biol Med. 2006 Oct 15;41(8):1304-14. Epub 2006 Jul 15.
RGD ID: 1641800
Pubmed: PMID:17015177   (View Abstract at PubMed)
DOI: DOI:10.1016/j.freeradbiomed.2006.07.011   (Journal Full-text)

The kallikrein/kinin system is beneficial in ischemia/reperfusion injury in heart, controversial in brain, but detrimental in lung, liver, and intestine. We examined the role of the kallikrein/kinin system in acute ischemia/reperfusion renal injury induced by 40 min occlusion of the renal artery followed by reperfusion. Rats were infused with tissue kallikrein protein 5 days before (pretreated group) or after (treated group) ischemia. Two days later, the pretreated group exhibited the worst renal dysfunction, followed by the treated group, then the control group. Kallikrein increased tubular necrosis and inflammatory cell infiltration with generation of more tumor necrosis factor-alpha and monocyte chemoattractant protein-1. Reactive oxygen species (ROS), malondialdehyde, and reduced/oxidized glutathione measurement revealed that the oxidative stress was augmented by kallikrein administration in both ischemic and reperfusion phases. The groups with more ROS generation also had more apoptotic renal cells. The deleterious effects of kallikrein on ischemia/reperfusion injury were reversed by cotreatment with bradykinin B2 receptor (B2R) antagonist, but not B1 receptor antagonist, and were not associated with hemodynamic changes. We conclude that early activation of B2R augmented ROS generation in ischemia/reperfusion renal injury, resulting in subsequent apoptosis, inflammation, and tissue damage. This finding suggests the potential application of B2R antagonists in acute ischemic renal disease associated with bradykinin activation.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
KLK1HumanInflammation  ISOKlk1 (Rattus norvegicus) RGD 
Klk1RatInflammation  IDA  RGD 
Klk1MouseInflammation  ISOKlk1 (Rattus norvegicus) RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Klk1Ratpositive regulation of acute inflammatory response  IMP  RGD 
Klk1Ratpositive regulation of apoptotic process  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Klk1  (kallikrein 1)

Genes (Mus musculus)
Klk1  (kallikrein 1)

Genes (Homo sapiens)
KLK1  (kallikrein 1)

Objects referenced in this article
Gene Klk1c12 kallikrein 1-related peptidase C12 Rattus norvegicus

Additional Information