RGD Reference Report - A synthetic peptide from transforming growth factor-beta1 type III receptor prevents myocardial fibrosis in spontaneously hypertensive rats. - Rat Genome Database

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A synthetic peptide from transforming growth factor-beta1 type III receptor prevents myocardial fibrosis in spontaneously hypertensive rats.

Authors: Hermida, N  Lopez, B  Gonzalez, A  Dotor, J  Lasarte, JJ  Sarobe, P  Borras-Cuesta, F  Diez, J 
Citation: Hermida N, etal., Cardiovasc Res. 2009 Feb 15;81(3):601-9. doi: 10.1093/cvr/cvn315. Epub 2008 Nov 19.
RGD ID: 8552780
Pubmed: PMID:19019833   (View Abstract at PubMed)
DOI: DOI:10.1093/cvr/cvn315   (Journal Full-text)

AIM: We investigated whether P144, a synthetic peptide from transforming growth factor-beta(1) (TGF-beta(1)) type III receptor betaglycan, exhibits cardiac antifibrotic properties. METHODS AND RESULTS: The study was carried out in one group of 10-week-old normotensive Wistar-Kyoto rats treated with vehicle (V-WKY), one group of 10-week-old spontaneously hypertensive rats treated with vehicle (V-SHR), and one group of 10-week-old SHR treated with P144 (P144-SHR) for 12 weeks. Two more groups of 10-week-old untreated WKY and SHR were used to assess baseline values of the parameters tested. In addition, the effects of P144 on rat cardiac fibroblasts stimulated with TGF-beta(1) were also studied. Compared with V-WKY, V-SHR exhibited significant increases in the myocardial expression of phosphorylated Smad2, 38 and 42 kDa connective tissue growth factor (CTGF) isoforms, procollagen alpha1 (I) mRNA, and collagen type I protein, as well as in the expression of lysyl oxidase (LOX) mRNA and protein, collagen cross-linking and deposition. P144 administration was associated with significant reduction in all these parameters in P144-SHR. TGF-beta(1)-stimulated fibroblasts exhibited significant increases in phosphorylated Smad2, 38 and 42 kDa CTGF proteins, and procollagen alpha(1) (I) mRNA compared with control fibroblasts. No significant differences were found in these parameters between fibroblasts incubated with TGF-beta(1) and P144 and control fibroblasts. CONCLUSION: These results show that P144 inhibits TGF-beta(1)-dependent signalling pathway and collagen type I synthesis in cardiac fibroblasts. These effects may be involved in the ability of this peptide to prevent myocardial fibrosis in SHR.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Cardiac Fibrosis treatmentISOCol1a1 (Rattus norvegicus)8552780; 8552780 RGD 
Cardiac Fibrosis treatmentIDA 8552780 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Col1a1  (collagen type I alpha 1 chain)

Genes (Mus musculus)
Col1a1  (collagen, type I, alpha 1)

Genes (Homo sapiens)
COL1A1  (collagen type I alpha 1 chain)


Additional Information