1
40
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Text
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URL Address
<a href="http://doi.org/10.1186/1475-2840-11-150" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/1475-2840-11-150</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
11-11
Volume
11
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Detecting Dna Synthesis Of Neointimal Formation After Catheter Balloon Injury In Gk And In Wistar Rats: Using 5-ethynyl-2 '-deoxyuridine
Publisher
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Cardiovascular Diabetology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-12
Subject
The topic of the resource
alkynes; arterial injury; balloon injury; Cardiovascular System & Cardiology; carotid-artery; Catheter; cell-cycle progression; click chemistry; diabetes-mellitus; diabetes-mellitus; DNA synthesis; EdU; eluting stents; Endocrinology & Metabolism; in-vitro; mammalian target; Neointimal formation; PCNA; proliferation; terminal
Creator
An entity primarily responsible for making the resource
Guo J S; Li D Y; Bai S R; Xu T D; Zhou Z M; Zhang Y B
Description
An account of the resource
Background: Neointimal formation plays an important role in the pathogenesis of coronary restenosis after percutaneous coronary intervention (PCI), especially in patients with diabetes mellitus. Recently, some studies have shown that 5-ethynyl-2'-deoxyuridine (EdU) incorporation can serve as a novel alternative to the 5-bromo-2'-deoxyuridine (BrdU) antibody detection method for detection of DNA synthesis in regenerating avian cochlea, chick embryo and the adult nervous system. However, few studies have been performed to assess the suitability of EdU for detecting DNA synthesis in vascular neointima. Methods: The carotid artery balloon injury model was established in Goto-Kakizaki (GK) and Wistar rats. A Cell-Light (TM) EdU Kit was used to detect EdU-labeled cell nuclei of common carotid arteries at day 7 after catheter balloon injury. Different methods of injecting EdU were tested. The protein levels of proliferating cell nuclear antigen (PCNA) and p-Akt (Ser473), as well as the mRNA levels of PCNA were evaluated by Western blotting and quantitative real-time PCR (qRT-PCR), respectively. Immunohistochemical staining was also employed to visualize PCNA-positive cells. Results: At day 7 after catheter balloon injury, far more EdU-positive and PCNA-positive cells were observed in GK rats. When comparing groups that received different EdU doses, it was found that the percentage of EdU-positive cells at a dose of 100 mg/kg body weight was than at doses of 25 mg/kg and 50 mg/kg. The number of positive cells was significantly higher in the repeated injection group compared to the single injection group. Further, after balloon injury DNA synthesis in GK rats was more notable than in Wistar rats. Neointimal formation in GK rats was more obvious than in Wistar rats. The protein levels of PCNA and p-Akt (Ser473) and the mRNA levels of PCNA were increased in injured rats as compared to uninjured rats, and were significantly higher in GK rats than in Wistar rats. Conclusion: By intraperitoneal injections of EdU at a dose of 100 mg/kg three times, EdU incorporation can detect carotid arterial DNA synthesis caused by neointimal formation in GK rats and Wistar rats at day 7 after balloon injury by the EdU click reaction quickly and effectively. Moreover, more obvious DNA synthesis in the vascular neointima could be observed in GK rats than in Wistar rats.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/1475-2840-11-150" target="_blank" rel="noreferrer noopener">10.1186/1475-2840-11-150</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
alkynes
arterial injury
Bai S R
balloon injury
Cardiovascular Diabetology
Cardiovascular System & Cardiology
carotid-artery
Catheter
cell-cycle progression
click chemistry
diabetes-mellitus
DNA synthesis
EdU
eluting stents
Endocrinology & Metabolism
Guo J S
in-vitro
Journal Article or Conference Abstract Publication
Li D Y
mammalian target
Neointimal formation
PCNA
proliferation
terminal
Xu T D
Zhang Y B
Zhou Z M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">http://doi.org/10.5551/jat.29421</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1317-1337
Issue
12
Volume
22
Search for Full-text
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Interleukin-1 Receptor-Associated Kinase 1/4 as a Novel Target for Inhibiting Neointimal Formation After Carotid Balloon Injury
Publisher
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Journal of Atherosclerosis and Thrombosis
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Cardiovascular System & Cardiology; in-vivo; smooth-muscle-cells; signaling pathways; hyperplasia; NF kappa B; arterial injury; bacterial infections; Carotid artery balloon injury; intimal; irak-4 protein; IRAK1/4; muscle cell; Neointimal formation; NF kappa B; TLR4; toll-like-receptor; toll-like-receptor-4 expression; Vascular smooth
Creator
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Bai S R; Li D Y; Zhou Z M; Cao J L; Xu T D; Zhang X T; Wang Y; Guo J S; Zhang Y B
Description
An account of the resource
Aim: Interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 play essential roles in the induction of inflammatory gene products. We aimed to investigate the effect of the inhibition of IRAK1 and IRAK4 kinase activities on neointimal formation in rats with carotid artery balloon injuries using the IRAK1/4 inhibitor N-(2-Morpholinylethyl)-2-(3-nitrobenzoylamido)-benzimidazole, a cell-permeable benzimidazole compound. Methods: Wistar rats and vascular smooth muscle cells (VSMCs) isolated from the thoracic aortas were used. Toll-like receptor 4 (TLR4)-mediated nuclear factor kappa B (NF kappa B) signaling pathway was revealed by microarrays analysis. In addition, the differential expression of the TLR4 pathway genes, including TLR4, IRAK1, I kappa B alpha, and interleukin-1 beta (IL-1 beta), was confirmed by quantitative real-time polymerase chain reaction. Immunohistochemical staining, elastic-van Gieson and Masson staining, 5-ethynyl-2'-deoxyuridine staining, enzyme-linked immunosorbent assay, transwell migration assay and western blotting were also contributed for relevant detection. Results: The expression of TLR4 protein gradually increased at days 1, 3, 7, and 21 after balloon injury compared with the uninjured group. The dual inhibition of IRAK1 and IRAK4 attenuated neointimal formation and fibrotic remodeling after injury in vivo and suppressed VSMC proliferation and migration in vitro. The production of mediators such as tumor necrosis factor-alpha and IL-1 beta in injured arteries were also reduced by the inhibition of IRAK1 and IRAK4. The expression of NF kappa B p65- and F4/80-positive cells in inhibitor rats were fewer than those in control rats at day 7, while IRAK1 expression was markedly higher at day 3 in inhibitor rats. Furthermore, western blotting analysis revealed that the IRAK1/4 inhibitor suppressed the IRAK1 and IRAK4 kinase activities and the activation of the TLR4-mediated NF kappa B pathway in vivo and in vitro. Conclusions: This study suggested that IRAK1/4 could serve as a potential therapeutic target to suppress neointimal formation in carotid arteries after balloon injury through the TLR4/NF kappa B signaling pathway.
Identifier
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<a href="http://doi.org/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">10.5551/jat.29421</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2015
arterial injury
Bacterial Infections
Bai S R
Cao J L
Cardiovascular System & Cardiology
Carotid artery balloon injury
Guo J S
Hyperplasia
in-vivo
intimal
irak-4 protein
IRAK1/4
Journal Article or Conference Abstract Publication
Journal of Atherosclerosis and Thrombosis
Li D Y
muscle cell
Neointimal formation
NF kappa B
signaling pathways
smooth-muscle-cells
TLR4
toll-like-receptor
toll-like-receptor-4 expression
Vascular smooth
Wang Y
Xu T D
Zhang X T
Zhang Y B
Zhou Z M