scholarly journals Dihydrotestosterone (DHT) increases cyclooxygenase‐2 (COX‐2) in human coronary artery smooth muscle cells following IL‐1β‐induced inflammation

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Kristen Osterlund ◽  
Anthony Gutierrez ◽  
Rayna J Gonzales
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclooxygenase 2 ◽  
Human Coronary Artery ◽  
Cox 2

scholarly journals Dihydrotestosterone alters cyclooxygenase-2 levels in human coronary artery smooth muscle cells

2010 ◽  
Vol 298 (4) ◽  
pp. E838-E845 ◽  
Author(s):  
Kristen L. Osterlund ◽  
Robert J. Handa ◽  
Rayna J. Gonzales
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Inflammatory Mediator ◽  
Physiological State ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Inflammatory Stimulus ◽  
Human Coronary Artery ◽  
Cox 2

Both protective and nonprotective effects of androgens on the cardiovascular system have been reported. Our previous studies show that the potent androgen receptor (AR) agonist dihydrotestosterone (DHT) increases levels of the vascular inflammatory mediator cyclooxygenase (COX)-2 in rodent cerebral arteries independent of an inflammatory stimulus. Little is known about the effects of androgens on inflammation in human vascular tissues. Therefore, we tested the hypothesis that DHT alters COX-2 levels in the absence and presence of induced inflammation in primary human coronary artery smooth muscle cells (HCASMC). Furthermore, we tested the ancillary hypothesis that DHT's effects on COX-2 levels are AR-dependent. Cells were treated with DHT (10 nM) or vehicle for 6 h in the presence or absence of LPS or IL-1β. Similar to previous observations in rodent arteries, in HCASMC, DHT alone increased COX-2 levels compared with vehicle. This effect of DHT was attenuated in the presence of the AR antagonist bicalutamide. Conversely, in the presence of LPS or IL-1β, increases in COX-2 were attenuated by cotreatment with DHT. Bicalutamide did not affect this response, suggesting that DHT-induced decreases in COX-2 levels occur independent of AR stimulation. Thus we conclude that DHT differentially influences COX-2 levels under physiological and pathophysiological conditions in HCASMC. This effect of DHT on COX-2 involves AR-dependent and- independent mechanisms, depending on the physiological state of the cell.

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.

scholarly journals Human Galectin-3 Promotes Trypanosoma cruzi Adhesion to Human Coronary Artery Smooth Muscle Cells

2004 ◽  
Vol 72 (11) ◽  
pp. 6717-6721 ◽  
Author(s):  
Yuliya Y. Kleshchenko ◽  
Tapria N. Moody ◽  
Vyacheslav A. Furtak ◽  
Josiah Ochieng ◽  
Maria F. Lima ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Trypanosoma Cruzi ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Human Cells ◽  
Human Coronary Artery ◽  
Dramatic Decrease ◽  
Galectin 3 ◽  
Initial Capacity

ABSTRACT Human galectin-3 binds to the surface of Trypanosoma cruzi trypomastigotes and human coronary artery smooth muscle (CASM) cells. CASM cells express galectin-3 on their surface and secrete it. Exogenous galectin-3 increased the binding of T. cruzi to CASM cells. Trypanosome binding to CASM cells was enhanced when either T. cruzi or CASM cells were preincubated with galectin-3. Cells stably transfected with galectin-3 antisense show a dramatic decrease in galectin-3 expression and very little T. cruzi adhesion to cells. The addition of galectin-3 to these cells restores their initial capacity to bind to trypanosomes. Thus, host galectin-3 expression is required for T. cruzi adhesion to human cells and exogenous galectin-3 enhances this process, leading to parasite entry.

scholarly journals Matrix metalloproteinases modulated by protein kinase Cε mediate resistin-induced migration of human coronary artery smooth muscle cells

2011 ◽  
Vol 53 (4) ◽  
pp. 1044-1051 ◽  
Author(s):  
Qinxue Ding ◽  
Hong Chai ◽  
Nausheen Mahmood ◽  
Jerry Tsao ◽  
Daria Mochly-Rosen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Matrix Metalloproteinases ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Human Coronary Artery
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