RGD Reference Report - Nanoparticle-mediated local delivery of an antisense TGF-beta1 construct inhibits intimal hyperplasia in autogenous vein grafts in rats. - Rat Genome Database

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Nanoparticle-mediated local delivery of an antisense TGF-beta1 construct inhibits intimal hyperplasia in autogenous vein grafts in rats.

Authors: Sun, DX  Liu, Z  Tan, XD  Cui, DX  Wang, BS  Dai, XW 
Citation: Sun DX, etal., PLoS One. 2012;7(7):e41857. doi: 10.1371/journal.pone.0041857. Epub 2012 Jul 30.
RGD ID: 7207219
Pubmed: PMID:22860019   (View Abstract at PubMed)
PMCID: PMC3408488   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0041857   (Journal Full-text)

BACKGROUND: Intimal hyperplasia is one of the most important causes of vascular graft failure. Numerous studies have correlated transforming growth factor-beta1 (TGF-beta1) with extracellular matrix (ECM) deposition, a hallmark of intimal thickening. PRINCIPAL FINDINGS: In the present study, we performed immunohistochemistry, RT-PCR, and Western blot to examine the dynamic expression of TGF-beta1, TGF-beta1 receptor type I (TGF-beta RI), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) during intimal hyperplasia in grafted veins of a rat model generated by grafting a portion of the right internal jugular vein to the ipisiliary carotid artery. Additionally, we determined whether nanoparticle-mediated delivery of a TGF-beta1 antisense-expressing construct prevented TGF-beta1 expression and intimal hyperplasia in grafted veins. In grafted veins, the expression of TGF-beta1 significantly increased on day 3 after transplantation, peaked on day 7, slightly decreased on day 14, and returned to baseline levels on day 28. The positive expression of TGF-beta RI in grafted veins remarkably increased on day 7, peaked on day 14, and decreased thereafter. MMP-1 expression decreased significantly, while TIMP-1 expression increased, significantly on days 14 and 28. Nanoparticle-mediated delivery of a TGF-beta1 antisense-expressing construct down-regulated TGF-beta1 expression and inhibited intimal hyperplasia in grafted veins. CONCLUSIONS: Our findings provide further evidence that TGF-beta1 plays an integral role in the development of intimal hyperplasia after vascular injury. Nanoparticle-mediated delivery of a TGF-beta1 antisense-expressing construct is a feasible strategy to target TGF-beta1-induced intimal thickening.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hyperplasia  ISOMmp1 (Rattus norvegicus)7207219; 7207219Intimal HyperplasiaRGD 
Hyperplasia  IDA 7207219Intimal HyperplasiaRGD 

Objects Annotated

Genes (Rattus norvegicus)
Mmp1  (matrix metallopeptidase 1)

Genes (Mus musculus)
Mmp1a  (matrix metallopeptidase 1a (interstitial collagenase))

Genes (Homo sapiens)
MMP1  (matrix metallopeptidase 1)


Additional Information