RGD Reference Report - Podocyte repopulation contributes to regression of glomerular injury induced by ACE inhibition. - Rat Genome Database

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Podocyte repopulation contributes to regression of glomerular injury induced by ACE inhibition.

Authors: Macconi, D  Sangalli, F  Bonomelli, M  Conti, S  Condorelli, L  Gagliardini, E  Remuzzi, G  Remuzzi, A 
Citation: Macconi D, etal., Am J Pathol. 2009 Mar;174(3):797-807. Epub 2009 Jan 22.
RGD ID: 2325229
Pubmed: PMID:19164508   (View Abstract at PubMed)
PMCID: PMC2665741   (View Article at PubMed Central)
DOI: DOI:10.2353/ajpath.2009.080227   (Journal Full-text)

Angiotensin-converting enzyme (ACE) inhibition induces glomerular repair in the Munich Wistar Fromter (MWF) rat, a model of spontaneous glomerular injury. In this study, we investigated whether this effect is related to changes in glomerular cell number, particularly of podocytes, which are progressively lost with age. MWF rats with advanced nephropathy were studied at both 40 weeks and after 20 weeks of observation either with or without treatment with the ACE inhibitor lisinopril. Forty-week-old Wistar rats were used as controls. In untreated MWF rats, proteinuria, hypertension, glomerulosclerosis, and renal function worsened, while lisinopril induced regression of both functional and structural changes. Despite glomerular hypercellularity in untreated MWF rats, the number of endothelial cells per glomerulus did not change, and podocyte number even decreased. ACE inhibition halted the progressive increase in glomerular cell number and enhanced endothelial cell volume density. Surprisingly, lisinopril not only halted age-related podocyte loss but also increased the number of glomerular podocytes above baseline, which was associated with an increased number of proliferating Wilms tumor 1-positive cells, loss of cyclin-dependent kinase inhibitor p27 expression, and increased number of parietal podocytes. These data indicate that ACE inhibition restructures glomerular capillary, primarily by restoring the podocyte population in this model of glomerular injury. Increased parietal podocyte number in lisinopril-treated MWF rats suggests that the remodeling of Bowman's capsule epithelial cells contributes to this effect.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ACEHumanglomerulonephritis  ISOAce (Rattus norvegicus) RGD 
AceRatglomerulonephritis  IMP  RGD 
AceMouseglomerulonephritis  ISOAce (Rattus norvegicus) RGD 
MWFRatproteinuria treatmentIAGPlisinoprilcompared to WKY and MWF 40 and 50 weeks and untreatedRGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MWFRatdecreased podocyte number treatmentIAGPlisinoprilcompared to WKY and MWF 40 weeks and untreatedRGD 
MWFRatglomerulosclerosis treatmentIAGPlisinoprilcompared to WKY and untreatedRGD 
MWFRathypertension treatmentIAGPlisinoprilcompared to WKY and untreatedRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ace  (angiotensin I converting enzyme)

Genes (Mus musculus)
Ace  (angiotensin I converting enzyme)

Genes (Homo sapiens)
ACE  (angiotensin I converting enzyme)

Strains
MWF  (NA)


Additional Information