• The Korean Journal of Physiology and Pharmacology
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• v.4 no.2
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• pp.105-111
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• 2000

Stimulation of muscarinic receptors by carbachol (CCh) in the circular smooth muscle of the guinea pig gastric antrum causes muscle contraction. In the present study, muscarinic receptor subtype controlling the muscle contraction in response to CCh was studied using putative muscarinic receptor antagonists. Isometric force of the isolated circular muscle strips was measured in an organ bath. CCh contracted the muscle in a dose-dependent way, and each of the three muscarinic receptor antagonists, 4-diphenylacetoxy- N-methylpeperdine methiodide (4-DAMP), methoctramine and pirenzepine shifted the concentration- response curves to the right without significantly reducing the maximum force. The affinities of the muscarinic antagonists $(pA_2\;values)$ obtained from Schild plot analysis were 10.15, 7.05 and 6.84 for 4-DAMP, methoctramine and pirenzepine, respectively. These results suggest that the $M_3-subtype$ mainly mediate the muscle contraction in response to CCh in guinea pig gastric antrum.

• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.113.1-113.1
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• 2006

• Journal of Korean Physical Therapy Science
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• v.13 no.2
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• pp.129-135
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• 2006

Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Go6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by $G{\ddot{o}}6976$. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC.

• Journal of Life Science
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• v.23 no.1
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• pp.137-142
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• 2013

Human adipose-derived mesenchymal stem cells (hMSCs) are highly useful for vascular regeneration of injured or inflamed tissue. Lipopolysaccharide (LPS) is a potent activator of macrophages and stimulates macrophages to release inflammatory cytokines. In the present study, we explored the role of LPS-activated macrophages in the differentiation of hMSCs to smooth muscle cells (SMCs). We demonstrated that conditioned medium from LPS-induced macrophages (LPS CM) stimulates differentiation of hMSCs to SMCs, as evidenced by increased expression of smooth muscle-specific markers, including alpha-smooth muscle actin (${\alpha}$-SMA), smooth muscle-myosin heavy chain, and calponin. LPS induced the secretion of $PGF2{\alpha}$ from macrophages, and $PGF2{\alpha}$ treatment stimulated expression levels of SMC-specific markers in hMSCs. Furthermore, small interfering RNA-mediated silencing of the $PGF2{\alpha}$ receptor inhibited LPS CM-stimulated ${\alpha}$-SMA expression. These results suggest that LPS-activated macrophages promote differentiation of hMSCs to SMCs through a $PGF2{\alpha}$-dependent mechanism.

• Tuberculosis and Respiratory Diseases
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• v.38 no.1
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• pp.8-15
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• 1991

It has been well known that the integrity of airway epithelium is important in development of bronchial hyperreactivity and bronchial asthma. But the mechanisms involved are still unclear. To evaluate that airway epithelium is able to modulate the contraction of guinea pig tracheal smooth muscle, we investigated the responsiveness of intact and epithelium-denuded tracheal strips to histamine and acetylcholine. And to evaluate whether cyclooxgenase products play a role in this modulatory mechanism, we also investigated the effect of indomethacin pretreatment on the tracheal responsiveness to histamine. Results were as follows: 1) In guinea pig tracheal smooth muscle the presence of airway epithelium significantly reduced the response to histamine. 2) In the presence of indomethacin dose-response curves and $EC_{50}$ values were similar between intact and epithelium-denuded tracheal strips, that is, indomethacin abolished the influence of epithelium on the contracion of tracheal smooth muscle. 3) The response of tracheal smooth muscle to acetylcholine was similar both in the presence and absence of epithelium. These results suggest that airway epithelium of guinea pig may generate an inhibitory signal to decrease the response of tracheal smooth muscle to histamine and cyclooxygenase products may contrbute to the modulation of airway epithelium on the contracion of tracheal smooth muscle.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.1060-1065
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• 2002

LC20 phosphorylation and PKC α play an important role in modulation of contractile activity of smooth muscle. Besides, myosin phosphatase is also related with smooth muscle contraction in signaling pathways. We previously demonstrated that Crataegi Fructus inhibited phenylephrine-induced contraction and which might be implicated in nitrite formation(Son et al., 2002). In this study, we investigated the effects of butanol fraction of Crataegi Fructus(BFFC) on the localization of α-protein kinease C(PKC α) and myosin phosphatase subnits(MPs) in freshly isolated single ferret potal vein cells, and phosphorylation of LC20 during phenylephrine stimulation. In PKC α and MPs localization, BFFC blocked its translocation from the cytosol to the cell membrane by treatment of phenylephrine. BFFC have also dephosphorylated LC20 phosphorylation by phenylephrine stimulation under basal level, but no significant. These results indicate that the relaxation effect of BFFC is associated with inhibition of PKC α activation and MPs dissociation, and thus myosin phosphatase activity may be increased.

• The Journal of Korean Medicine
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• v.25 no.4
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• pp.108-120
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• 2004

Objective : Euonymus alatus (Thunb.) Sieb (EA) is a traditional Korean herbal medicine, commonly used to treat tumors in Korea and China for centuries. Several earlier studies have indicated that EA exhibits anti-tumor properties, but its mechanism remains to be elucidated. In this study, we evaluated the molecular mechanism of EA in a human uterine leiomyomal smooth muscle cell (ULSMC) line. Methods : This study was evaluated by: (a), morphological changes by using acridine orange/ethidium bromide staining; (b), DNA fragmentation by TdT-mediated dUTP nick end labeling (TUNEL); and (c), sub-G1 cell analysis. Results : This study observed that EA treatment caused apoptotic cell death and depletion of intracellular glutathione (GSH) and that reduction of mitochondrial membrane potential was found to be involved in the initiation of apoptosis by EA. Conclusion : This results show that EA exerted clear cytotoxic effects and strongly inhibited the proliferation of ULSMC.

• Journal of Nutrition and Health
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• v.49 no.1
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• pp.59-62
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• 2016

Purpose: Zinc, a biomineral present within and outside cells, manages various cellular mechanisms. In this study, we examined whether zinc was involved in vascular smooth muscle cell (VSMC) calcification via regulation of calcification inhibitor protein, osteopontin (OPN). Methods: Rat aorta cell line (A7r5 cells) and primary vascular smooth muscle cells (pVSMCs) from rat aorta were cultured with phosphate (1-5 mM) and zinc ($0-15{\mu}M$) as appropriate, along with osteoblasts (MC3T3-E1) as control. The cells were then stained for Ca and P deposition for calcification examination as well as osteopontin expression as calcification inhibitor protein was measured. Results: Both Ca and phosphate deposition increased as the addition of phosphate increased. In the same manner, the expression of osteopontin was upregulated as the addition of phosphate increased in both cell types. When zinc was added, Ca and P deposition decreased in VSMCs, while it increased in osteoblasts. Conclusion: The results imply that zinc may prevent VSMC calcification by stimulating calcification inhibitor protein OPN synthesis in VSMCs.

• Journal of Veterinary Clinics
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• v.23 no.4
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• pp.421-426
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• 2006

The effects of transmural nerve stimulation induced releasing neurotransmitters on the changes of swine uterine smooth muscle motility were examined by polygraph through isometric force transducer. The frequency dependent relaxation and rebound contraction were revealed on precontraction with histamine by transmural nerve stimulation. The rebound contraction by transmural nerve stimulation was inhibited by nonselective ${\alpha}$-adrenergic receptor antagonist, phentolamine, and the relaxation by transmural nerve stimulation was blocked by nonselective ${\beta}$-adrenergic receptor antagonist, propranolol. The relaxation induced by nonselective ${\beta}$-adrenergic receptor agonist, isoproterenol on precontraction with histamine were the dose dependent manner and this relaxation was blocked by nonselective ${\beta}$-adrenergic receptor antagonist, propranolol in isolated uterine smooth muscle of pig. These results suggest that endogenous neurotransmitters on smooth muscle relaxation was influenced by ${\beta}$-adrenergic receptor in swine.

• Korean Journal of Veterinary Service
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• v.18 no.3
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• pp.29-35
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• 1995

The effects of prostaglandin $F_2{\alpha}$ were investigated on the uterine smooth muscle motility in the pig. The results were summarized as follows : 1. Prostaglandin $F_2{\alpha}$ caused the contraction of the porcine uterine smooth muscle and the contractile responses increased between the concentration of prostaglandine $F_2{\alpha}$ $10^{-9}$ M and $5{\times}10^{-8}$ M with a dose-dependent manner. 2. The contractile response induced by prostaglandine $F_2{\alpha}$($10^{-8}$ M) was not blocked by pre-treatment with cholinergic receptor blocker, atropine ($10^{-6}$ M). 3. The contractile response induced by prostaglandine $F_2{\alpha}$(10$^{-8}$ M) was not blocked by pretreament with ${\alpha}$-adrenergic receptor blocker, phentolamine($10^{-6}$ M) and ${\beta}$-adrenergic receptor blocker, propranolol($10^{-6}$ M). From these results, it was concluded that the effects of uterine smooth muscle by prostaglandine $F_2{\alpha}$ were only the contraction mediated by prostaglandine TEX>$F_2{\alpha}$ receptor in pig, and that it may not be related to the cholinergic and adrenergic receptor.