RGD Reference Report - Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model. - Rat Genome Database

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Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model.

Authors: Chung, JH  Choi, HJ  Kim, SY  Hong, KS  Min, SK  Nam, MH  Kim, CW  Koh, YH  Seo, JB 
Citation: Chung JH, etal., BMC Genomics. 2011 Oct 20;12:520. doi: 10.1186/1471-2164-12-520.
RGD ID: 11041642
Pubmed: PMID:22014063   (View Abstract at PubMed)
PMCID: PMC3209477   (View Article at PubMed Central)
DOI: DOI:10.1186/1471-2164-12-520   (Journal Full-text)

BACKGROUND: To investigate the molecular and cellular pathogenesis underlying myocarditis, we used an experimental autoimmune myocarditis (EAM)-induced heart failure rat model that represents T cell mediated postinflammatory heart disorders. RESULTS: By performing unbiased 2-dimensional electrophoresis of protein extracts from control rat heart tissues and EAM rat heart tissues, followed by nano-HPLC-ESI-QIT-MS, 67 proteins were identified from 71 spots that exhibited significantly altered expression levels. The majority of up-regulated proteins were confidently associated with unfolded protein responses (UPR), while the majority of down-regulated proteins were involved with the generation of precursor metabolites and energy metabolism in mitochondria. Although there was no difference in AKT signaling between EAM rat heart tissues and control rat heart tissues, the amounts and activities of extracellular signal-regulated kinase (ERK)-1/2 and ribosomal protein S6 (rpS6) were significantly increased. By comparing our data with the previously reported myocardial proteome of the Coxsackie viruses of group B (CVB)-mediated myocarditis model, we found that UPR-related proteins were commonly up-regulated in two murine myocarditis models. Even though only two out of 29 down-regulated proteins in EAM rat heart tissues were also dysregulated in CVB-infected rat heart tissues, other proteins known to be involved with the generation of precursor metabolites and energy metabolism in mitochondria were also dysregulated in CVB-mediated myocarditis rat heart tissues, suggesting that impairment of mitochondrial functions may be a common underlying mechanism of the two murine myocarditis models. CONCLUSIONS: UPR, ERK-1/2 and S6RP signaling were activated in both EAM- and CVB-induced myocarditis murine models. Thus, the conserved components of signaling pathways in two murine models of acute myocarditis could be targets for developing new therapeutic drugs or methods aimed at treating enigmatic myocarditis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
RPS6HumanExperimental Autoimmune Myocarditis  ISORps6 (Rattus norvegicus) RGD 
Rps6RatExperimental Autoimmune Myocarditis  IDA  RGD 
Rps6MouseExperimental Autoimmune Myocarditis  ISORps6 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Rps6  (ribosomal protein S6)

Genes (Mus musculus)
Rps6  (ribosomal protein S6)

Genes (Homo sapiens)
RPS6  (ribosomal protein S6)


Additional Information