Epothilone D, a microtubule-stabilizing compound, inhibits neointimal hyperplasia after rat carotid artery injury by cell cycle arrest via regulation of G1-checkpoint proteins

2007 ◽  
Vol 47 (4) ◽  
pp. 229-237 ◽  
Author(s):  
Tack-Joong Kim ◽  
Yong Lim ◽  
Dong-Woon Kim ◽  
Jin-Sook Kwon ◽  
Ju-Hee Son ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Carotid Artery ◽  
Cell Cycle Arrest ◽  
Neointimal Hyperplasia ◽  
Carotid Artery Injury ◽  
Checkpoint Proteins ◽  
Artery Injury ◽  
Cycle Arrest ◽  
Epothilone D ◽  
G1 Checkpoint

scholarly journals Fission Yeast Rad26 Is a Regulatory Subunit of the Rad3 Checkpoint Kinase

2002 ◽  
Vol 13 (2) ◽  
pp. 480-492 ◽  
Author(s):  
Tom D. Wolkow ◽  
Tamar Enoch
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Fission Yeast ◽  
Complex Analysis ◽  
Kinase Activity ◽  
Regulatory Subunit ◽  
Kinase Activation ◽  
Checkpoint Proteins ◽  
Cycle Arrest ◽  
Phosphoinositide 3 Kinase

Fission yeast Rad3 is a member of a family of phosphoinositide 3-kinase -related kinases required for the maintenance of genomic stability in all eukaryotic cells. In fission yeast, Rad3 regulates the cell cycle arrest and recovery activities associated with the G2/M checkpoint. We have developed an assay that directly measures Rad3 kinase activity in cells expressing physiological levels of the protein. Using the assay, we demonstrate directly that Rad3 kinase activity is stimulated by checkpoint signals. Of the five other G2/M checkpoint proteins (Hus1, Rad1, Rad9, Rad17, and Rad26), only Rad26 was required for Rad3 kinase activity. Because Rad26 has previously been shown to interact constitutively with Rad3, our results demonstrate that Rad26 is a regulatory subunit, and Rad3 is the catalytic subunit, of the Rad3/Rad26 kinase complex. Analysis of Rad26/Rad3 kinase activation in rad26.T12, a mutant that is proficient for cell cycle arrest, but defective in recovery, suggests that these two responses to checkpoint signals require quantitatively different levels of kinase activity from the Rad3/Rad26 complex.

scholarly journals Bortezomib Reduces Neointimal Hyperplasia in a Rat Carotid Artery Injury Model

2013 ◽  
Vol 43 (9) ◽  
pp. 592
Author(s):  
Ki-Seok Kim ◽  
Song Yi Kim ◽  
Joon Hyeok Choi ◽  
Seung Jae Joo ◽  
Dong Woon Kim ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Neointimal Hyperplasia ◽  
Carotid Artery Injury ◽  
Artery Injury ◽  
Injury Model

scholarly journals Characterization of G1 checkpoint control in the yeast Saccharomyces cerevisiae following exposure to DNA-damaging agents.

Genetics ◽  
1994 ◽  
Vol 138 (2) ◽  
pp. 271-281 ◽  
Author(s):  
W Siede ◽  
A S Friedberg ◽  
I Dianova ◽  
E C Friedberg
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
S Phase ◽  
Checkpoint Control ◽  
Cycle Arrest ◽  
Dna Damaging Agents ◽  
Nucleotide Excision ◽  
G1 Checkpoint

Abstract The delay of S-phase following treatment of yeast cells with DNA-damaging agents is an actively regulated response that requires functional RAD9 and RAD24 genes. An analysis of cell cycle arrest indicates the existence of (at least) two checkpoints for damaged DNA prior to S-phase; one at START (a G1 checkpoint characterized by pheromone sensitivity of arrested cells) and one between the CDC4- and CDC7-mediated steps (termed the G1/S checkpoint). When a dna1-1 mutant (that affects early events of replicon initiation) also carries a rad9 deletion mutation, it manifests a failure to arrest in G1/S following incubation at the restrictive temperature. This failure to execute regulated G1/S arrest is correlated with enhanced thermosensitivity of colony-forming ability. In an attempt to characterize the signal for RAD9 gene-dependent G1 and G1/S cell cycle arrest, we examined the influence of the continued presence of unexcised photoproducts. In mutants defective in nucleotide excision repair, cessation of S-phase was observed at much lower doses of UV radiation compared to excision-proficient cells. However, this response was not RAD9-dependent. We suggest that an intermediate of nucleotide excision repair, such as DNA strand breaks or single-stranded DNA tracts, is required to activate RAD9-dependent G1 and G1/S checkpoint controls.

scholarly journals Peroxisome Proliferator-Activated ReceptorαPlays an Important Role in the Expression of Monocyte Chemoattractant Protein-1 and Neointimal Hyperplasia after Vascular Injury

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Yu Peng ◽  
Qiang Li ◽  
Lu Zhang ◽  
Ming Bai ◽  
Zheng Zhang
Keyword(s):  
Carotid Artery ◽  
Neointimal Hyperplasia ◽  
Peroxisome Proliferator ◽  
Neointimal Formation ◽  
Carotid Artery Injury ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Artery Injury

Peroxisome proliferator-activated receptorαis a member of the nuclear receptor superfamily. It modulates smooth muscle cell proliferation and inflammatory cytokines in vitro. In this study, we tested the hypothesis that PPARαwould decrease the expression of monocyte chemoattractant protein-1 and tissue factor, and inhibit neointimal formation in a murine double carotid artery injury model. Carotid artery injury was performed in the PPARαknockout and wild type (WT) mice, treated and untreated with Wy14643, a PPARαactivator. Up-regulated MCP-1 and TF expression and more neointimal formation were observed in the PPARα−/−mice compared with WT mice. The activation of PPARαresulted in further decreased neointimal formation. Our data further suggest that the decrease in neointimal formation is due to down-regulation of MCP-1 by PPARαresulting in decreased leukocyte infiltration and TF expression.

Effect of Local Administration of Lovastatin on Preventing Neointimal Hyperplasia in the Rat Carotid Artery Injury Model

1999 ◽  
Vol 29 (8) ◽  
pp. 812
Author(s):  
Sang Chol Lee ◽  
Duk Kyung Kim ◽  
Seung Woo Park ◽  
Jeong Eun Huh ◽  
Sun Jin Park ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Neointimal Hyperplasia ◽  
Local Administration ◽  
Carotid Artery Injury ◽  
Artery Injury ◽  
Injury Model

Abstract 455: Fimasartan Reduced Carotid Atherosclerosis Progression After Mechanical Injury in ApoE Knockout Mouse

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Jong-Ho Kim ◽  
I-Rang Lim ◽  
Hyung Joon Joo ◽  
Seung-Cheol Choi ◽  
Soon Jun Hong
Keyword(s):  
Carotid Artery ◽  
Neointimal Hyperplasia ◽  
Carotid Artery Injury ◽  
Atherosclerosis Progression ◽  
Artery Injury ◽  
Group 4 ◽  
Group 3 ◽  
Group 2 ◽  
Apoe Knockout Mouse ◽  
Group 1

Aim: The beneficial effects of angiotensin receptor blockers (ARBs) in atherosclerosis have been demonstrated in numerous studies. We investigated the effects of fimasartan in reducing atherosclerosis progression and systemic inflammation after carotid artery injury in ApoE knockout mouse. Methods: Male ApoE knockout mice were randomly allocated to Group 1 (without carotid artery injury, n =20), Group 2 (without carotid artery injury + fimasartan, n =21), Group 3 (carotid artery injury, n =25) and Group 4 (carotid artery injury + fimasartan, n =24). Fimasartan (3mg/kg in distilled water) was orally injected on daily basis, and left carotid artery injury was induced with 0.014 inch guidewire. At 28 days, hematoxylin & eosin and elastic stains were used to measure cross-sectional atherosclerotic plaque from carotid artery. Moreover, inflammatory markers such as MMP9, IL-6, TNFα and ICAM were analyzed by ELISA, and anti-inflammatory cytokines such as IL-10 was measured in peripheral blood. Results: Histomorphometric staining showed significantly reduced neointimal hyperplasia in Group 2 (2.30±0.66%) compared to Group 1 (12.31±2.97%, p <0.05). In addition, Group 4 (32.03±4.62%) showed significantly reduced neointimal hyperplasia compared to Group 3 (50.06±7.50%, p <0.05). All fimasartan treated groups revealed decreased smooth muscle cell proliferation and CD68+ macrophages in carotid artery. Furthermore, inflammatory cytokines such as MMP9 and IL-6 were significantly lower in Group 4 (0.32±0.02ng/mL and 11.68±2.13pg/mL) compared to Group 3 (0.54±0.13ng/mL and 16.68±3.03pg/mL, p <0.05, respectively). In particular, TNFα and ICAM at were significantly decreased in Group 2 (5.83±2.28pg/mL and 3.76±0.84ng/mL) and Group 4 (7.32±0.95pg/mL and 5.04±1.47ng/mL) compared to Group 1 (6.64±1.34pg/mL and 4.42±0.88ng/mL) and Group 3 (9.28±1.57pg/mL and 6.31±1.60ng/mL, p <0.05, respectively). IL-10 increased significantly in Group 4 (29.20±0.52pg/mL) compared to Group 3 (26.18±1.14pg/mL, p <0.05). Conclusions: Fimasartan reduced neointimal hyperplasia with decreases in macrophages in carotid atherosclerotic plaque and with reductions in systemic inflammation in ApoE knockout mice.

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