RGD Reference Report - Elevated levels of activin A in heart failure: potential role in myocardial remodeling. - Rat Genome Database

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Elevated levels of activin A in heart failure: potential role in myocardial remodeling.

Authors: Yndestad, A  Ueland, T  Oie, E  Florholmen, G  Halvorsen, B  Attramadal, H  Simonsen, S  Froland, SS  Gullestad, L  Christensen, G  Damas, JK  Aukrust, P 
Citation: Yndestad A, etal., Circulation. 2004 Mar 23;109(11):1379-85. Epub 2004 Mar 1.
RGD ID: 1580888
Pubmed: PMID:14993131   (View Abstract at PubMed)
DOI: DOI:10.1161/01.CIR.0000120704.97934.41   (Journal Full-text)

BACKGROUND: Although modulation of inflammatory processes has been suggested as a new treatment modality in heart failure (HF), our knowledge about abnormalities in the cytokine network during HF is still limited. On the basis of a previous cDNA array study examining peripheral blood mononuclear cells from HF patients, we hypothesized a role for activin A, a member of the transforming growth factor (TGF)-beta superfamily, in the pathogenesis of HF. METHODS AND RESULTS: This study had 4 main and novel findings. First, serum levels of activin A were significantly elevated in patients with HF (n=86) compared with healthy control subjects (n=20), with increasing levels according to disease severity as assessed by clinical, hemodynamic, and neurohormonal parameters. Second, compared with control subjects, HF patients, as determined by real-time quantitative reverse transcriptase polymer chain reaction, also had markedly increased gene expression of the activin A subunit activin betaA in T cells but not in monocytes. Third, in a rat model of HF, we demonstrated a concerted induction of the gene expression of activin betaA and activin receptors IA, IB, IIA, and IIB after myocardial infarction. Immunohistochemical analysis localized activin A solely to cardiomyocytes. Finally, activin A markedly increased gene expression of mediators involved in infarction healing and myocardial remodeling (ie, atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, transforming growth factor-beta1, and monocyte chemoattractant protein-1) in neonatal rat cardiomyocytes. CONCLUSIONS: Together with our demonstration of activin A-induced gene expression in neonatal cardiomyocytes of mediators related to myocardial remodeling, the expression pattern of activin A during clinical and experimental HF suggests an involvement of this cytokine in the pathogenesis of HF.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
INHBAHumancongestive heart failure severityIEP mRNA more ...RGD 
InhbaRatcongestive heart failure severityISOINHBA (Homo sapiens)mRNA more ...RGD 
InhbaMousecongestive heart failure severityISOINHBA (Homo sapiens)mRNA more ...RGD 
INHBAHumanmyocardial infarction  ISOInhba (Rattus norvegicus)mRNA:increased expression:heart (rat)RGD 
InhbaRatmyocardial infarction  IEP mRNA:increased expression:heart (rat)RGD 
InhbaMousemyocardial infarction  ISOInhba (Rattus norvegicus)mRNA:increased expression:heart (rat)RGD 
ACVR1BHumanMyocardial Ischemia  ISOAcvr1b (Rattus norvegicus) RGD 
Acvr1bRatMyocardial Ischemia  IEP  RGD 
Acvr1bMouseMyocardial Ischemia  ISOAcvr1b (Rattus norvegicus) RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
InhbaRatcytokine-mediated signaling pathway  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Acvr1b  (activin A receptor type 1B)
Inhba  (inhibin subunit beta A)

Genes (Mus musculus)
Acvr1b  (activin A receptor, type 1B)
Inhba  (inhibin beta-A)

Genes (Homo sapiens)
ACVR1B  (activin A receptor type 1B)
INHBA  (inhibin subunit beta A)


Additional Information