RGD Reference Report - The mannose-binding lectin-pathway is involved in complement activation in the course of renal ischemia-reperfusion injury. - Rat Genome Database

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The mannose-binding lectin-pathway is involved in complement activation in the course of renal ischemia-reperfusion injury.

Authors: De Vries, B  Walter, SJ  Peutz-Kootstra, CJ  Wolfs, TG  Van Heurn, LW  Buurman, WA 
Citation: de Vries B, etal., Am J Pathol. 2004 Nov;165(5):1677-88.
RGD ID: 6903263
Pubmed: PMID:15509537   (View Abstract at PubMed)
PMCID: PMC1618654   (View Article at PubMed Central)
DOI: DOI:10.1016/S0002-9440(10)63424-4   (Journal Full-text)

Ischemia-reperfusion (I/R) is an important cause of acute renal failure (ARF). The complement system appears to be essentially involved in I/R injury. However, via which pathway the complement system is activated and in particular whether the mannose-binding lectin (MBL)-pathway is activated is unclear. This tempted us to study the activation and regulation of the MBL-pathway in the course of experimental renal I/R injury and in clinical post-transplant ARF. Mice subjected to renal I/R displayed evident renal MBL-depositions, depending on the duration of warm ischemia, in the early reperfusion phase. Renal deposition of C3, C6 and C9 was observed in the later reperfusion phase. The deposition of MBL-A and -C completely co-localized with the late complement factor C6, showing that MBL is involved in complement activation in the course of renal I/R injury. Moreover, the degree of early MBL-deposition correlated with complement activation, neutrophil-influx, and organ-failure observed in the later reperfusion phase. In serum of mice subjected to renal I/R MBL-A, levels increased in contrast to MBL-C levels, which dropped evidently. In line, liver mRNA levels for MBL-A increased, whereas MBL-C levels decreased. Renal MBL mRNA levels rapidly dropped in the course of renal I/R. Finally, in human biopsies, MBL-depositions were observed early after transplantation of ischemically injured kidneys. In line with our experimental data, in ischemically injured grafts displaying post-transplant organ-failure extensive MBL depositions were observed in peritubular capillaries and tubular epithelial cells. In conclusion, in experimental renal I/R injury and clinical post-transplant ARF the MBL-pathway is activated, followed by activation of the complement system. These data indicate that the MBL-pathway is involved in ischemia-induced complement activation.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MBL2HumanReperfusion Injury  ISOMbl2 (Mus musculus)protein:increased expression:serumRGD 
Mbl1RatReperfusion Injury  ISOMbl1 (Mus musculus)protein:decreased expression:serumRGD 
Mbl1MouseReperfusion Injury  IEP protein:decreased expression:serumRGD 
Mbl2RatReperfusion Injury  ISOMbl2 (Mus musculus)protein:increased expression:serumRGD 
Mbl2MouseReperfusion Injury  IEP protein:increased expression:serumRGD 

Objects Annotated

Genes (Rattus norvegicus)
Mbl1  (mannose binding lectin 1)
Mbl2  (mannose binding lectin 2)

Genes (Mus musculus)
Mbl1  (mannose-binding lectin (protein A) 1)
Mbl2  (mannose-binding lectin (protein C) 2)

Genes (Homo sapiens)
MBL2  (mannose binding lectin 2)


Additional Information