RGD Reference Report - Recombinant human erythropoietin pretreatment alleviates renal glomerular injury induced by cardiopulmonary bypass by reducing transient receptor potential channel 6-nuclear factor of activated T-cells pathway activation. - Rat Genome Database

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Recombinant human erythropoietin pretreatment alleviates renal glomerular injury induced by cardiopulmonary bypass by reducing transient receptor potential channel 6-nuclear factor of activated T-cells pathway activation.

Authors: Liu, X  Zhang, T  Xia, W  Wang, Y  Ma, K 
Citation: Liu X, etal., J Thorac Cardiovasc Surg. 2013 Mar 24. pii: S0022-5223(13)00274-2. doi: 10.1016/j.jtcvs.2013.02.076.
RGD ID: 7247439
Pubmed: PMID:23535151   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jtcvs.2013.02.076   (Journal Full-text)

OBJECTIVE: Acute renal injury after cardiopulmonary bypass is common and associated with high mortality. We aimed to demonstrate the glomerular protective effects of recombinant human erythropoietin using an in vivo rat cardiopulmonary bypass model and to explore the possible mechanism. METHODS: Dose-related renal protective effects of recombinant human erythropoietin were studied in phase I. Male Sprague Dawley rats were randomly divided into 5 groups: sham group, cardiopulmonary bypass group, and 3 recombinant human erythropoietin-treated cardiopulmonary bypass groups (bolus doses of 500, 3000, and 5000 U/kg 24 hours before surgery). Blood and urine samples were collected just before surgery and at 2, 4, 24, 48, and 72 hours after surgery. In phase II, rats were divided into 3 groups: sham group, cardiopulmonary bypass group, and 5000 U/kg recombinant human erythropoietin group. Kidneys were harvested at 4, 24, 48, and 72 hours after surgery. Ultra-organization of glomeruli was observed. Glomerular transient receptor potential channel 6 (TRPC6) expression was studied by immunofluorescence and Western blot. Nuclei nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) activity was analyzed by enzyme-linked immunosorbent assays and electrophoretic mobility shift assay. RESULTS: Pretreatment of 5000 U/kg recombinant human erythropoietin decreased the urine protein (72 hours: 7.82 +/- 1.13 g/L vs 11.28 +/- 1.73 g/L), serum creatinine (72 hours: 35.0 +/- 3.5 mumol/L vs 60.7 +/- 7.6 mumol/L), and cystatin-C (2 hours: 336.5 +/- 28.2 mug/L vs 452.6 +/- 63.8 mug/L) compared with the control group (P < .01). Cardiopulmonary bypass induced morphologic abnormalities of podocyte foot processes and slit diaphragms, which was improved by recombinant human erythropoietin. Furthermore, recombinant human erythropoietin significantly relieved glomerular TRPC6 increase and NFATc1 activation induced by cardiopulmonary bypass. CONCLUSIONS: Pretreatment of 5000 U/kg recombinant human erythropoietin elicited potent glomerular protection against cardiopulmonary bypass. This protection may be partly due to downregulation of glomerular TRPC6-NFATc1 pathway.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
NFATC1Humankidney disease treatmentISONfatc1 (Rattus norvegicus)associated with Postoperative ComplicationsRGD 
Nfatc1Mousekidney disease treatmentISONfatc1 (Rattus norvegicus)associated with Postoperative ComplicationsRGD 
Nfatc1Ratkidney disease treatmentIEP associated with Postoperative ComplicationsRGD 
TRPC6Humankidney disease treatmentISOTrpc6 (Rattus norvegicus) RGD 
Trpc6Ratkidney disease treatmentIDA  RGD 
Trpc6Mousekidney disease treatmentISOTrpc6 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nfatc1  (nuclear factor of activated T-cells 1)
Trpc6  (transient receptor potential cation channel, subfamily C, member 6)

Genes (Mus musculus)
Nfatc1  (nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1)
Trpc6  (transient receptor potential cation channel, subfamily C, member 6)

Genes (Homo sapiens)
NFATC1  (nuclear factor of activated T cells 1)
TRPC6  (transient receptor potential cation channel subfamily C member 6)


Additional Information