• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.623-630
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• 1999

Decreased cardiac contractility occurs in endotoxicosis, but little is known about the ionic mechanism responsible for myocardial dysfunction. In this study, we examined the changes in $Ca{2+}$ and $K^+$ currents in cardiac myocytes from endotoxin-treated rat. Ventricular myocytes were isolated from normal and endotoxemic rats (ex vivo), that were treated for 10 hours with Salmonella enteritidis lipopolysaccharides (LPS; 1.5 mg/kg) intravenously. Normal cardiac myocytes were also incubated for 6 hours with 200 ng/ml LPS (in vitro). L-type $Ca{2+}$ current $(I_{Ca,L})$ and transient outward $K^+$ current $(I_{to})$ were measured using whole cell patch clamp techniques. Peak $I_{Ca,L}$ was reduced in endotoxemic myocytes (ex vivo; 6.00.4 pA/pF, P＜0.01) compared to normal myocytes (control; 10.90.6 pA/pF). Exposure to endotoxin in vitro also attenuated $I_{Ca,L}$ (8.40.4 pA/pF, P＜0.01). The amplitude of $(I_{to})$ on depolarization to 60 mV was reduced in endotoxin treated myocytes (16.51.5 pA/pF, P＜0.01, ex vivo; 20.00.9 pA/pF, P＜0.01 , in vitro) compared to normal myocytes (control; 24.71.0 pA/pF). There was no voltage shift in steady-state inactivation of $I_{Ca,L}$ and $(I_{to})$ between groups. These results suggest that endotoxin reduces $Ca{2+}$ and $K^+$ currents of rat cardiac myocytes, which may lead to cardiac dysfunction.

• Journal of Mechanical Science and Technology
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• 제20권5호
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• pp.668-674
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• 2006

In order to develop a cell based robot, we present a micro-mechanical force measurement system for the biological muscle actuators, which utilize glucose as a power source. The proposed measurement system is composed of a micro-manipulator, a force transducer with a glass probe, a signal processor, an inverted microscope and video recording system. Using this measurement system, the contractile force and frequency of the cardiac myocytes were measured in real time and the magnitudes of the contractile force of each cardiac myocyte under different conditions were compared. From the quantitative experimental results, we could estimate that the force of cardiac myocytes is about $20\sim40{\mu}N$, and show that there are differences between the control cells and the micro-patterned cells.

• The Korean Journal of Physiology and Pharmacology
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• 제28권4호
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• pp.335-344
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• 2024

Diphenyleneiodonium (DPI) has been widely used as an inhibitor of NADPH oxidase (Nox) to discover its function in cardiac myocytes under various stimuli. However, the effects of DPI itself on Ca²⁺ signaling and contraction in cardiac myocytes under control conditions have not been understood. We investigated the effects of DPI on contraction and Ca²⁺ signaling and their underlying mechanisms using video edge detection, confocal imaging, and whole-cell patch clamp technique in isolated rat cardiac myocytes. Application of DPI suppressed cell shortenings in a concentration-dependent manner (IC₅₀ of ≅0.17 µM) with a maximal inhibition of ~70% at ~100 µM. DPI decreased the magnitude of Ca²⁺ transient and sarcoplasmic reticulum Ca²⁺ content by 20%-30% at 3 µM that is usually used to remove the Nox activity, with no effect on fractional release. There was no significant change in the half-decay time of Ca²⁺ transients by DPI. The L-type Ca²⁺ current (I_Ca) was decreased concentration-dependently by DPI (IC₅₀ of ≅40.3 µM) with ≅13.1%-inhibition at 3 µM. The frequency of Ca²⁺ sparks was reduced by 3 µM DPI (by ~25%), which was resistant to a brief removal of external Ca²⁺ and Na⁺. Mitochondrial superoxide level was reduced by DPI at 3-100 µM. Our data suggest that DPI may suppress L-type Ca²⁺ channel and RyR, thereby attenuating Ca²⁺-induced Ca²⁺ release and contractility in cardiac myocytes, and that such DPI effects may be related to mitochondrial metabolic suppression.

• 약학회지
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• 제54권1호
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• pp.8-12
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• 2010

Inositol 1,4,5-trisphosphate ($IP_3$) receptor ($IP_3R$)-mediated signaling pathway is involved in many cellular processes including fertilization, apoptosis and neuronal function. Although cardiac myocytes express the $IP_3R$, its pathophysiological role has not been clearly understood because of limited selectivity of currently available pharmacological blockers. In the present study we constructed shRNA-expressing adenovirus to knock-down the type 2 $IP_3R$ ($IP_3R2$), a major subtype in cardiac ventricular myocytes, and demonstrated that the virus successfully eliminated the expression and localization of the $IP_3R2$. These results may provide a reliable tool for probing pathophysiological roles of the $IP_3R2$ in isolated intact cardiac myocytes.

• 약학회지
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• 제28권3호
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• pp.129-138
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• 1984

Specific [$^{3}H$] ouabain binding and $Ca^{2+}$ -uptake were measured to elucidate the role of high affinity [$^{3}H$] ouabain binding site in rat cardiac myocytes which contain 65% of rod cells. High affinity [$^{3}$H] ouabain binding site, which is about 3% of total pump sites, with apparent dissociation constant ($K_{D}$) of $1.1{\times}10^{-7}M$ and maximum binding site concentration (Bmax) of 1.2 pmol/mg protein ($1.754{\times}10^{5}cells$) were identified. At the concentration of $10^{-7}M$ to $10^{-4}M$, ouabain produced concentration dependent increase in $Ca^{2+}$-uptake of myocytes. The effect of ouabain on $Ca^{2+}$-uptake was not effected by membrane depolarization (elevated K+ in incubation medium) or verapamil. These results suggest that in rat ventricular myocytes the ouabain receptor complex to high affinity site may increase Na+ - $Ca^{2+}$ exchange across the sarcolemmal membrane by inhibition of Na+, K+ - ATPase.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
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• pp.24-25
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• 1999

Intracellular pH(pH$_{i}$) regulation is very important to regulate the cellular functions of cardiac myocytes such as contractility, signal transduction, ion regulation, cell volume, and energy production etc. The resting pH$_{i}$ was maintained at about 7.07 and strictly regulated within the range of $\pm$0.1.(omitted)ted)

• 제어로봇시스템학회:학술대회논문집
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• 제어로봇시스템학회 2005년도 ICCAS
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• pp.1179-1182
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• 2005

To facilitate the cell based robot research, we presented a micro-mechanical force measurement system for the biological muscle actuators, which utilize glucose as a power source for potential application in a human body or blood vessels. The system is composed of a micro-manipulator, a force transducer with a glass probe, a signal processor, an inverted microscope and video recoding system. Using this measurement system, the contractile force and frequency of the cardiac myocytes were measured in real time and the magnitude of the contractile force of each cardiac myocyte on a different condition was compared. From the quantitative experimental results, we estimated that the force of cardiac myocytes is about $20{\sim}40\;{\mu}$N, and showed that there is difference between the control cells and the micro-patterned cells.

• 약학회지
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• 제59권4호
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• pp.158-163
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• 2015

Cardiac myocytes are subjected to fluid shear stress during each contraction and relaxation. Under pathological conditions, such as valve disease, heart failure or hypertension, shear stress in cardiac chamber increases due to high blood volume and pressure. The shear stress induces proarrhythmic longitudinal global $Ca^{2+}$ waves in atrial myocytes. In the present study, we further explored underlying cellular mechanism for the shear stress-induced longitudinal global $Ca^{2+}$ wave in isolated rat atrial myocytes. A shear stress of ${\sim}16dyn/cm^2$ was applied onto entire single myocyte using pressurized fluid puffing. Confocal $Ca^{2+}$ imaging was performed to measure local and global $Ca^{2+}$ signals. Shear stress elicited longitudinally propagating global $Ca^{2+}$ wave (${\sim}80{\mu}m/s$). The occurrence of shear stress-induced atrial $Ca^{2+}$ wave was eliminated by the inhibition of ryanodine receptors (RyRs) or inositol 1,4,5-trisphosphate receptors ($IP_3Rs$). In addition, pretreatment of phospholipase C (PLC) inhibitor U73122, but not its inactive analogue U73343, abolished the generation of longitudinal $Ca^{2+}$ wave under shear stress. Our data suggest that shear-induced longitudinal $Ca^{2+}$ wave may be induced by $Ca^{2+}$-induced $Ca^{2+}$ release through the RyRs which is triggered by $PLC-IP_3R$ signaling in atrial myocytes.

• Biomolecules & Therapeutics
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• 제24권1호
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• pp.19-24
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• 2016

Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. The exploration of new biomarkers with high sensitivity and specificity for early diagnosis of AMI therefore becomes one of the primary task. In the current study, we aim to detect whether there is any heart specific long noncoding RNA (lncRNA) releasing into the circulation during AMI, and explore its function in the neonatal rat cardiac myocytes injury induced by $H_2O_2$. Our results revealed that the cardiac-specific lncRNA MHRT (Myosin Heavy Chain Associated RNA Transcripts) was significantly elevated in the blood from AMI patients compared with the healthy control ($^*p<0.05$). Using an in vitro neonatal rat cardiac myocytes injury model, we demonstrated that lncRNA MHRT was upregulated in the cardiac myocytes after treatment with hydrogen peroxide ($H_2O_2$) via real-time RT-PCR (qRT-PCR). Furthermore, we knockdowned the MHRT gene by siRNA to confirm its roles in the $H_2O_2$-induced cardiac cell apoptosis, and found that knockdown of MHRT led to significant more apoptotic cells than the non-target control ($^{**}p<0.01$), indicating that the lncRNA MHRT is a protective factor for cardiomyocyte and the plasma concentration of MHRT may serve as a biomarker for myocardial infarction diagnosis in humans AMI.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.17-17
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• 2001

It is well known that myocardial stretch causes changes in electrical signalling and contractility of the heart. For example, mechanical stretch depolarises the membrane potential of cardiac cells and alters the shape of action potentials. As a result, these effects either accelerate the frequency of heart rate or induce arrhythmias of the heart.(omitted)