RGD Reference Report - Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice. - Rat Genome Database

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Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice.

Authors: Yang, Yongyao  Tang, Feng  Wei, Fang  Yang, Long  Kuang, Chunyan  Zhang, Hongming  Deng, Jiusheng  Wu, Qiang 
Citation: Yang Y, etal., Aging (Albany NY). 2019 Nov 22;11(22):10016-10030. doi: 10.18632/aging.102388. Epub 2019 Nov 22.
RGD ID: 242905202
Pubmed: PMID:31757932   (View Abstract at PubMed)
PMCID: PMC6914395   (View Article at PubMed Central)
DOI: DOI:10.18632/aging.102388   (Journal Full-text)

This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression. H19 was capable of recruiting CTCF to suppress PKD1, thus promoting atherosclerotic vulnerable plaque formation and intraplaque angiogenesis in atherosclerosis mice. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
H19Ratatherosclerosis amelioratesISOH19 (Mus musculus)ApoE knockout miceRGD 
H19Humanatherosclerosis amelioratesISOH19 (Mus musculus)ApoE knockout miceRGD 
H19Mouseatherosclerosis amelioratesIMP ApoE knockout miceRGD 
MMP2Humanatherosclerosis amelioratesISOMmp2 (Mus musculus) RGD 
Mmp2Ratatherosclerosis amelioratesISOMmp2 (Mus musculus) RGD 
Mmp2Mouseatherosclerosis amelioratesIDA  RGD 
TIMP1Humanatherosclerosis amelioratesISOTimp1 (Mus musculus) RGD 
TP53Humanatherosclerosis amelioratesISOTrp53 (Mus musculus) RGD 
Timp1Ratatherosclerosis amelioratesISOTimp1 (Mus musculus) RGD 
Timp1Mouseatherosclerosis amelioratesIDA  RGD 
Tp53Ratatherosclerosis amelioratesISOTrp53 (Mus musculus) RGD 
Trp53Mouseatherosclerosis amelioratesIDA  RGD 
VEGFAHumanatherosclerosis amelioratesISOVegfa (Mus musculus) RGD 
VegfaRatatherosclerosis amelioratesISOVegfa (Mus musculus) RGD 
VegfaMouseatherosclerosis amelioratesIDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
H19  (H19 imprinted maternally expressed transcript)
Mmp2  (matrix metallopeptidase 2)
Timp1  (TIMP metallopeptidase inhibitor 1)
Tp53  (tumor protein p53)
Vegfa  (vascular endothelial growth factor A)

Genes (Mus musculus)
H19  (H19, imprinted maternally expressed transcript)
Mmp2  (matrix metallopeptidase 2)
Timp1  (tissue inhibitor of metalloproteinase 1)
Trp53  (transformation related protein 53)
Vegfa  (vascular endothelial growth factor A)

Genes (Homo sapiens)
H19  (H19 imprinted maternally expressed transcript)
MMP2  (matrix metallopeptidase 2)
TIMP1  (TIMP metallopeptidase inhibitor 1)
TP53  (tumor protein p53)
VEGFA  (vascular endothelial growth factor A)


Additional Information