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
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
congestive heart failure severityIEP 1580888mRNA more ...RGD 
congestive heart failure severityISOINHBA (Homo sapiens)1580888; 1580888mRNA more ...RGD 
myocardial infarction  ISOInhba (Rattus norvegicus)1580888; 1580888mRNA:increased expression:heart (rat)RGD 
myocardial infarction  IEP 1580888mRNA:increased expression:heart (rat)RGD 
Myocardial Ischemia  ISOAcvr1b (Rattus norvegicus)1580888; 1580888 RGD 
Myocardial Ischemia  IEP 1580888 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cytokine-mediated signaling pathway  IEP 1580888 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