RGD Reference Report - Quantitative proteomic profiling identifies new renal targets of copper(II)-selective chelation in the reversal of diabetic nephropathy in rats. - Rat Genome Database

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Quantitative proteomic profiling identifies new renal targets of copper(II)-selective chelation in the reversal of diabetic nephropathy in rats.

Authors: Gong, D  Chen, X  Middleditch, M  Huang, L  Vazhoor Amarsingh, G  Reddy, S  Lu, J  Zhang, S  Ruggiero, K  Phillips, AR  Cooper, GJ 
Citation: Gong D, etal., Proteomics. 2009 Sep;9(18):4309-20. doi: 10.1002/pmic.200900285.
RGD ID: 10003054
Pubmed: PMID:19634143   (View Abstract at PubMed)
DOI: DOI:10.1002/pmic.200900285   (Journal Full-text)

This study aimed to identify new diabetic nephropathy (DN)-related proteins and renal targets of the copper(II)-selective chelator, triethylenetetramine (TETA) in streptozotocin-diabetic rats. We used the recently developed iTRAQ technology to compare renal protein profiles among non-diabetic, diabetic, and TETA-treated diabetic rats. In diabetic kidneys, tubulointerstitial nephritis antigen (TINag), voltage-dependent anion-selective channel (VDAC) 1, and VDAC2 were up-regulated in parallel with alterations in expression of proteins with functions in oxidative stress and oxidative phosphorylation (OxPhos) pathways. By contrast, mitochondrial HSP 60, Cu/Zn-superoxide dismutase, glutathione S-transferase alpha3 and aquaporin-1 were down-regulated in diabetic kidneys. Following TETA treatment, levels of D-amino acid oxidase-1, epoxide hydrolase-1, aquaporin-1, and a number of mitochondrial proteins were normalized, with concomitant amelioration of albuminuria. Changes in levels of TINag, collagen VIalpha1, actinin 4alpha, apoptosis-inducing factor 1, cytochrome C, histone H3, VDAC1, and aquaporin-1 were confirmed by Western blotting or immunohistochemistry. Changes in expression of proteins related to tubulointerstitial function, podocyte structure, and mitochondrial apoptosis are implicated in the mechanism of DN and their reversal by TETA. These findings are consistent with the hypothesis that this new experimental therapy may be useful for treatment of DN.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Diabetes Mellitus  ISOVdac1 (Rattus norvegicus)10003054; 10003054protein:increased expression:kidneyRGD 
Experimental Diabetes Mellitus  IEP 10003054protein:increased expression:kidneyRGD 

Objects Annotated

Genes (Rattus norvegicus)
Vdac1  (voltage-dependent anion channel 1)

Genes (Mus musculus)
Vdac1  (voltage-dependent anion channel 1)

Genes (Homo sapiens)
VDAC1  (voltage dependent anion channel 1)


Additional Information