scholarly journals Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10344
Author(s):  
Mingming Yang ◽  
Caroline Dart ◽  
Tomoko Kamishima ◽  
John M. Quayle
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Coronary Artery ◽  
Oxidative Phosphorylation ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Metabolic Inhibitors ◽  
Human Coronary Artery ◽  
Ideal Candidate ◽  
Hypoxic Vasodilation

ATP-sensitive potassium (KATP) channels couple cellular metabolism to excitability, making them ideal candidate sensors for hypoxic vasodilation. However, it is still unknown whether cellular nucleotide levels are affected sufficiently to activate vascular KATP channels during hypoxia. To address this fundamental issue, we measured changes in the intracellular ATP:ADP ratio using the biosensors Perceval/PercevalHR, and membrane potential using the fluorescent probe DiBAC4(3) in human coronary artery smooth muscle cells (HCASMCs). ATP:ADP ratio was significantly reduced by exposure to hypoxia. Application of metabolic inhibitors for oxidative phosphorylation also reduced ATP:ADP ratio. Hyperpolarization caused by inhibiting oxidative phosphorylation was blocked by either 10 µM glibenclamide or 60 mM K+. Hyperpolarization caused by hypoxia was abolished by 60 mM K+ but not by individual K+ channel inhibitors. Taken together, these results suggest hypoxia causes hyperpolarization in part by modulating K+ channels in SMCs.

ATP activates K and Cl channels via purinoceptor-mediated release of Ca2+ in human coronary artery smooth muscle

1996 ◽  
Vol 271 (5) ◽  
pp. C1463-C1471 ◽  
Author(s):  
D. Strobaek ◽  
P. Christophersen ◽  
S. Dissing ◽  
S. P. Olesen
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Receptor Agonist ◽  
Muscle Cells ◽  
Receptor Activation ◽  
Bk Channels ◽  
Bk Channel ◽  
Human Coronary Artery

Coronary artery smooth muscle cells express G protein-coupled purinoceptors, and we report here for the first time how receptor activation by extracellular ATP influences cell membrane currents and membrane potential in human cells. ATP (100 microM) stimulated a triphasic change in membrane potential lasting several seconds, which was caused by sequential opening of transient inward and outward conductances. The inward current was carried by Cl- and the outward current by K+, as shown by ion substitution and changes in holding potential. Both currents were independent of the presence of external Ca2+ but were blocked by strong buffering of Ca2+ in the internal solution. The P2u- and P2y-purinoceptor agonists UTP and 2-methylthioadenosine 5'-triphosphate activated similar currents, whereas the P2x-receptor agonist alpha, beta-methyleneadenosine 5'-triphosphate and the P1-receptor agonist adenosine failed to stimulate any whole cell currents. The ATP-activated K+ current was inhibited by iberiotoxin (200 nM), and it was potentiated by the BK channel activator NS-1619 (30 microM). In cell-attached recordings, ATP activated a 230-pS BK channel. In conclusion, ATP acting via P2 purinoceptors stimulated release of Ca2+ from internal stores and transiently activated depolarizing Cl- and hyperpolarizing BK channels in human coronary artery smooth muscle cells.

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

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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