RGD Reference Report - Protective Role of Testosterone in Ischemia-Reperfusion-induced Acute Kidney Injury. - Rat Genome Database

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Protective Role of Testosterone in Ischemia-Reperfusion-induced Acute Kidney Injury.

Authors: Soljancic, A  Lopez Ruiz, AF  Chandrashekar, K  Maranon, RO  Liu, R  Reckelhoff, JF  Juncos, LA 
Citation: Soljancic A, etal., Am J Physiol Regul Integr Comp Physiol. 2013 Apr 3.
RGD ID: 7244372
Pubmed: PMID:23552495   (View Abstract at PubMed)
PMCID: PMC4074000   (View Article at PubMed Central)
DOI: DOI:10.1152/ajpregu.00360.2012   (Journal Full-text)

Men are at greater risk for renal injury and dysfunction after acute ischemia-reperfusion (I/R) than are women. Studies in animals suggest that the reason for the sex difference in renal injury and dysfunction after I/R is the protective effect of estrogens in females. However, a reduction in testosterone in men is thought to play an important role in mediating cardiovascular and renal disease in general. In the present study we tested the hypothesis that I/R of the kidney reduces serum testosterone and that contributes to renal dysfunction and injury. Male rats that were subjected to renal ischemia of 40 min followed by reperfusion had a 90% reduction in serum testosterone by 3 hrs post reperfusion that remained at 24 hr. Infusion of testosterone 3 hrs after reperfusion attenuated the increase in plasma creatinine and urinary kidney injury molecule-1 (KIM-1) at 24 hrs, prevented the reduction in outer medullary blood flow, attenuated the increase in intrarenal TNF-alpha, and the decrease in intrarenal vascular endothelial growth factor at 48 hrs. Castration of males caused greater increases in plasma creatinine and KIM-1 at 24 hrs than in intact males with renal I/R, and treatment with anastrozole, an aromatase inhibitor, plus testosterone almost normalized plasma creatinine and KIM-1 in rats with renal I/R. These data show that renal I/R is associated with sustained reductions in testosterone, that testosterone repletion protects the kidney whereas castration promotes renal dysfunction and injury, and that the testosterone-mediated protection is not conferred by conversion to estradiol.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Kidney Reperfusion Injury treatmentISOCyp19a1 (Rattus norvegicus)7244372; 7244372 RGD 
Kidney Reperfusion Injury treatmentIMP 7244372 RGD 
Kidney Reperfusion Injury  ISOHavcr1 (Rattus norvegicus)7244372; 7244372protein:increased expression:urine:RGD 
Kidney Reperfusion Injury  IEP 7244372protein:increased expression:urine:RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to testosterone  IEP 7244372 RGD 

Cellular Component
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
extracellular space  IDA 7244372 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cyp19a1  (cytochrome P450, family 19, subfamily a, polypeptide 1)
Havcr1  (hepatitis A virus cellular receptor 1)

Genes (Mus musculus)
Cyp19a1  (cytochrome P450, family 19, subfamily a, polypeptide 1)
Havcr1  (hepatitis A virus cellular receptor 1)

Genes (Homo sapiens)
CYP19A1  (cytochrome P450 family 19 subfamily A member 1)
HAVCR1  (hepatitis A virus cellular receptor 1)


Additional Information