RGD Reference Report - Stimulated activation of platelet-derived growth factor receptor in vivo in balloon-injured arteries: a link between angiotensin II and intimal thickening. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Stimulated activation of platelet-derived growth factor receptor in vivo in balloon-injured arteries: a link between angiotensin II and intimal thickening.

Authors: Abe, J  Deguchi, J  Matsumoto, T  Takuwa, N  Noda, M  Ohno, M  Makuuchi, M  Kurokawa, K  Takuwa, Y 
Citation: Abe J, etal., Circulation. 1997 Sep 16;96(6):1906-13.
RGD ID: 11087557
Pubmed: PMID:9323080   (View Abstract at PubMed)

BACKGROUND: Growth factors such as platelet-derived growth factor (PDGF) have been postulated to be important mediators of neointimal formation in balloon-injured artery. Binding of growth factors to their receptors activates intrinsic receptor tyrosine kinase, resulting in tyrosine phosphorylation of receptors themselves and cellular substrate proteins. We investigated in vivo activities of growth factors by determining the extent of tyrosine phosphorylation of growth factor receptors and substrate proteins in injured artery. METHODS AND RESULTS: Rat balloon-injured carotid artery was analyzed for phosphotyrosine content of PDGF alpha- and beta-receptors, epidermal growth factor (EGF) receptors, and insulin receptor substrate-1 (IRS-1) by immunoprecipitation and anti-phosphotyrosine Western blot. The development of intimal thickening after deendothelializing balloon catheterization of rat carotid artery was accompanied by transient twofold to threefold increases in the extent of tyrosyl phosphorylation of PDGF alpha- and beta-receptors but not EGF receptor or IRS-1. The AT1 angiotensin II (Ang II) receptor antagonist TCV-116 markedly inhibited both tyrosyl phosphorylation of PDGF alpha- and beta-receptors and intimal thickening. The AT1 antagonist reduced mRNA levels of both PDGF-A and -B chains in injured arteries. CONCLUSIONS: The present study provides direct evidence for increased PDGF activities in injured artery in situ and the involvement of Ang II in stimulated activation of PDGF receptors. These results are consistent with the pathogenetic role for PDGF in intimal thickening.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Neointima treatmentISOPdgfra (Rattus norvegicus)11087557; 11087557associated with Carotid Artery InjuriesRGD 
Neointima treatmentISOPdgfrb (Rattus norvegicus)11087557; 11087557associated with Carotid Artery InjuriesRGD 
Neointima treatmentIEP 11087557; 11087557associated with Carotid Artery InjuriesRGD 

Objects Annotated

Genes (Rattus norvegicus)
Pdgfra  (platelet derived growth factor receptor alpha)
Pdgfrb  (platelet derived growth factor receptor beta)

Genes (Mus musculus)
Pdgfra  (platelet derived growth factor receptor, alpha polypeptide)
Pdgfrb  (platelet derived growth factor receptor, beta polypeptide)

Genes (Homo sapiens)
PDGFRA  (platelet derived growth factor receptor alpha)
PDGFRB  (platelet derived growth factor receptor beta)


Additional Information