scholarly journals Cytostatic Activity of Paclitaxel in Coronary Artery Smooth Muscle Cells is Mediated Through Transient Mitotic Arrest Followed by Permanent Post-Mitotic Arrest: Comparison with Cancer Cells

Cell Cycle ◽  
2006 ◽  
Vol 5 (14) ◽  
pp. 1574-1579 ◽  
Author(s):  
Mikhail V. Blagosklonny ◽  
Zoya N. Demidenko ◽  
Maria Giovino ◽  
Carmin Szynal ◽  
Elina Donskoy ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Cancer Cells ◽  
Muscle Cells ◽  
Mitotic Arrest ◽  
Cytostatic Activity

Abciximab Inhibits the Migration and Invasion Potential of Human Coronary Artery Smooth Muscle Cells

2000 ◽  
Vol 32 (12) ◽  
pp. 2195-2206 ◽  
Author(s):  
Rüdiger Blindt ◽  
Anja-Katrin Bosserhoff ◽  
Ute Zeiffer ◽  
Nicole Krott ◽  
Peter Hanrath ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Migration And Invasion ◽  
Human Coronary Artery ◽  
Invasion Potential

Effects of Vitamin D analogs on gene expression profiling in human coronary artery smooth muscle cells

2006 ◽  
Vol 186 (1) ◽  
pp. 20-28 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
Masaki Nakane ◽  
Junli Ma ◽  
Xiaoan Ruan ◽  
Paul E. Kroeger
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Muscle Cells ◽  
Human Coronary Artery ◽  
Vitamin D Analogs

scholarly journals Effects of Serum Amyloid A and Lysophosphatidylcholine on Intracellular Calcium Concentration in Human Coronary Artery Smooth Muscle Cells

2011 ◽  
Vol 52 (3) ◽  
pp. 185-193 ◽  
Author(s):  
Tomofumi Tanaka ◽  
Kenichi Ikeda ◽  
Yumiko Yamamoto ◽  
Haruko Iida ◽  
Hironobu Kikuchi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Serum Amyloid A ◽  
Muscle Cells ◽  
Serum Amyloid ◽  
Human Coronary Artery ◽  
Amyloid A

scholarly journals Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

2018 ◽  
Vol 50 (4) ◽  
pp. 1301-1317 ◽  
Author(s):  
Hongmei Li ◽  
Xian Wang ◽  
Anlong Xu
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Human Coronary Artery ◽  
Post Intervention ◽  
Inflammatory Activation ◽  
Myd88 Pathway

Background/Aims: Approximately 10%-20% of patients with acute cardiovascular disease who have received coronary intervention suffer restenosis and high inflammation. The stent compound paclitaxel+hirudin was prepared for the treatment of post-intervention restenosis. This study aimed to explore the anti-inflammatory and anti-restenosis mechanisms of paclitaxel+hirudin with regard to the TLR4/MyD88/NF-κB pathway. Methods: Human coronary artery smooth muscle cells (HCASMCs) at 4-6 generations after in vitro culture were used as a model. Lipopolysaccharide (LPS) was used as an inducer to maximally activate the TLR4/MyD88/NF-κB inflammation pathway. After MyD88 knockdown and selective blocking of MyD88 degradation with epoxomicin, the effects of paclitaxel+hirudin stenting on key sites of the TLR4/MyD88/NF-κB pathway were detected using ELISA, Q-PCR, and western blot analysis. Results: LPS at 1 μg/mL for 48 h was the optimal modeling condition for inflammatory activation of HCASMCs. Paclitaxel+hirudin inhibited the levels of key proteins and the gene expression, except for that of the MyD88 gene, of the TLR4-MyD88 pathway. The trend of the effect of paclitaxel+hirudin on the pathway proteins was similar to that of MyD88 knockdown. After epoxomicin intervention, the inhibitory effects of paclitaxel+hirudin on the key genes and proteins of the TLR4-MyD88 pathway were significantly weakened, which even reached pre-intervention levels. Paclitaxel+hirudin affected the MyD88 protein in a dosage-dependent manner. Conclusion: The paclitaxel+hirudin compound promotes MyD88 degradation in the TLR4/MyD88/NF-κB pathway to reduce the activity of TLR4 and NF-κB p65 and to weaken the LPS-initiated inflammatory reactions of IL-1β, IL-6, and TNF-α.

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