• The Korean Journal of Zoology
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• v.36 no.3
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• pp.433-438
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• 1993

In the previous paper (Choi et al., 1992), we found that a large but transient elevation in intracellular cGMP levels occur concomitant with the myoblast fusion. To establish the physiological significance of the elevation of cGMP levels, the change in guanylate cyclase activity dudng myoblast fusion and the correlation hetween various chemicals that may affect guanylate cyclase adivity and myoblast fusion were examined. Sodium nitroprusside, a nitric oxide-forming compound, induced a precocious fusion and increased guanylate cyclase activity compared to the control. Furthermore, L-NG-monomethyl arginine, specific inhibitor of L-arginine: nitric oxide synthase, inhibited the cell fusion in a dose-dependent manner, without affecting biochemical differentiation. On the basis of our present findings, we propose that the onset of myoblast fusion is somehow correlated with the rise in cellular cGMP levels that is regulated by the activation or inhibItIon of soluble guanylate cyclase, via as yet undefined mechanism but possibly through L-arginine: nitric oxide pathway.

• The Korean Journal of Zoology
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• v.36 no.3
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• pp.347-352
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• 1993

N-ethylmaleimide at low concentrations is known to interact specifically with 2 sulfhydryl residues in myosin heavy chain. Calpain, a Ca$^2$+-dependent neutral protease isolated from chick skeletal muscle, was found to preferentially degrade the alkylated protein but much less significantly the unmodified protein. Exposure of myosin to KMnO$_4$, which is also known to interact with sulthydryl groups, also caused the rapid degradation of the myosin heavy chain. Furthermore, treatment of each agent with increasing concentrations results in a greater loss of the myosin ATPase activity, indicating that the modification occurred at the reactive site sulfhydryl residues. These results suggest that the covalent modification at the reactive site salfhydryl residues in the myosin heavy chain may mark the protein for degradation by intracellular proteases such as calpain.

• The Korean Journal of Zoology
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• v.36 no.3
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• pp.342-346
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• 1993

The protein level of cytoskeletons in cultured myoblasts was found to gradually decrease during the course of myogenesis. This decrease, however, could be prevented by treatiag the ceils with calpeptin (benzyloxycarbonyl-Leu-nLeu-H), a cell penetrating inhibitor of calpain. In contrast, E-64, which also is a potent inhibitor of calpain but can not be transported into the cells, showed little or no effect. In addition, the treatment of calpeptin was found to stabilize a number of specific cytoskeletal proteins from degradation but without any effect on the pattern of total cells proteins. Furthermore, calpeptin, but not E-64, blocked myoblast fusion in a dose-dependent manner. These results suggest that calpain is responsible for the myogenic time-dependent loss of cytoskeletal proteins and that the degradative process is associated with myoblast fusion. These results also suggest that the differential effects of the calpain inhibitors depend on the permeabIlity of the drugs across the cell membrane.

• Journal of the Korean Chemical Society
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• v.35 no.1
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• pp.3-15
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• 1991

The gaseous mixtures of iso-propanol of 10 torr with carbon dioxide of 0∼1990 torr were irradiated with Co-60 gamma radiation up to 50 kGy, and the products such as carbon monoxide, acetone, methane, ethane, C$_3$H$_a$, C$_4$H$_b$ and tert-butanol were analyzed by gas chromatography. G(CO) value of 4 was obtained from the gas mixtures containing more than 490 torr of carbon dioxide. The production rates of the organic products and the decomposition rate of iso-propanol increased linearly with the pressure of carbon dioxide, and G(-iso-Propanol) and G(Acetone) values increased by 4 and 2, respectively, with each 10 torr increment of carbon dioxide pressure. The mechanisms of the radiolytic decomposition of iso-propanol and the production of carbon monoxide and organic materials are discussed on the basis of the experimental results of the present study.

• The Korean Journal of Zoology
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• v.27 no.2
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• pp.73-84
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• 1984

In order to investigate the effect of neurotransmitter on myoblast differentiation in vitro, the effects of dopamine and epinephrine on myoblast fusion and on the intracellular cAMP level in cultured myoblasts were examined. Dopamine $(3\\times10^{-5}M)$ and epinephrine $(3\\times10^{-5}M)$, when added at 34 hr after cell plating, markedly inhibited myoblast fusion, and dopamine was more potent than epinephrine. Both dopamine and epinephrine had no effect on intracellular cAMP level. At the same time, exogeneous dbcAMP, $PGE_1$, and aspirin were used to examine whether cAMP is involved in myoblast differentiation. dbcAMP $(1\\times10^{-4}M)$ inhibited myoblast fusion, whereas $PGE_1 (3\\times10^{-6}M)$ had no inhibitory effect, rather enhancing myoblast fusion. Aspirin, an inhibitor of PG synthetase, was shown to inhibit myoblast fusion. Possible mechanism by which dopamine or epinephrine at a specific concentration used inhibits myoblast fusion is discussed.

• Molecules and Cells
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• v.22 no.3
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• pp.353-359
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• 2006

The bone morphogenetic protein (BMP) family has been implicated in control of cartilage development. Here, we demonstrate that BMP-2 promotes chondrogenesis by activating p38 mitogen-activated protein kinase (MAPK), which in turn downregulates $Wnt-7a/{\beta}$-catenin signaling responsible for proteasomal degradation of Sox9. Exposure of mesenchymal cells to BMP-2 resulted in upregulation of Sox9 protein and a concomitant decrease in the level of ${\beta}$-catenin protein and Wnt-7a signaling. In agreement with this, the interaction of Sox9 with ${\beta}$-catenin was inhibited in the presence of BMP-2. Inhibition of the p38 MAPK pathway using a dominant negative mutant led to sustained Wnt-7a signaling and decreased Sox9 expression, with consequent inhibition of precartilage condensation and chondrogenic differentiation. Moreover, overexpression of ${\beta}$-catenin caused degradation of Sox9 via the ubiquitin/26S proteasome pathway. Our results collectively indicate that the increase in Sox9 protein resulting from downregulation of ${\beta}$-catenin/Wnt-7a signaling is mediated by p38 MAPK during BMP-2 induced chondrogenesis in chick wing bud mesenchymal cells.

• The Korean Journal of Pharmacology
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• v.13 no.1 s.21
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• pp.13-21
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• 1977

The author confirmed the development of the smooth muscle in the oviduct proprius and anterior mesosalpinx in the leghorn, and observed that there was a variation between the action of norepinephrine on albumin-secreting portion of productive oviduct and that of non-productive one, and that $PGE_1$ might play a significant role on the activation of adrenergic ${\alpha}$-receptor in the non-productive oviduct. 1. There were many bundles of smooth muscles with irregular directions, which were identified in the both oviduct proprius and anterior mesosalpinx by Mallory aniline-blue orange G stain. 2. In vitro experiments, the anterior mesosalpinx was always relaxed by norepinephrine. While the albumin-secreting portion of non-productive period of oviduct was relaxed, but that of the productive one contracted by norepinephrine. Both the anterior mesosalpinx and oviduct proprius of chick responsed with relaxation to norepinephrine as shown in the non-productive hen. In vivo experiments, norepinephrine injected through the jugular vein increased the intraoviductal pressure in the productive oviduct, but decreased that in the non-productive one. 3. By treatment with $PGE_1$, in vitro, the relaxation induced not only by norepinephrine, but by periarterial electrical stimulation was converted into contraction, and in the presence of phentolamine, this conversion by $PGE_1$ was not shown. 4. The intra-oviductal pressure of the productive hen treated with indomethacin for 4 days was decreased by norepinephrine, but the increase in pressure by $PGE_1$ or $PGE_{2{\alpha}}$ was supersensitized when these drugs were administered through jugular vein. However, in vivo, the relaxation by norepinephrine was not converted into the stimulation after $PGE_1$ treatment. It might be summarized that the regulation of intra-oviductal pressure was dependent on the summation of the movement of both oviduct and mesosalpinx and intramurally produced prostaglandins contributes to the inherent tone of the prcductive oviduct by activating adrenergic ${\alpha}$-receptor.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.5
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• pp.267-274
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• 2008

Since first discovered in chick skeletal muscles, stretch-activated channels (SACs) have been proposed as a probable mechano-transducer of the mechanical stimulus at the cellular level. Channel properties have been studied in both the single-channel and the whole-cell level. There is growing evidence to indicate that major stretch-induced changes in electrical activity are mediated by activation of these channels. We aimed to investigate the mechanism of stretch-induced automaticity by exploiting a recent mathematical model of rat atrial myocytes which had been established to reproduce cellular activities such as the action potential, $Ca^{2+}$ transients, and contractile force. The incorporation of SACs into the mathematical model, based on experimental results, successfully reproduced the repetitive firing of spontaneous action potentials by stretch. The induced automaticity was composed of two phases. The early phase was driven by increased background conductance of voltage-gated $Na^+$ channel, whereas the later phase was driven by the reverse-mode operation of $Na^+/Ca^{2+}$ exchange current secondary to the accumulation of $Na^+$ and $Ca^{2+}$ through SACs. These results of simulation successfully demonstrate how the SACs can induce automaticity in a single atrial myocyte which may act as a focus to initiate and maintain atrial fibrillation in concert with other arrhythmogenic changes in the heart.

• Journal of radiological science and technology
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• v.25 no.2
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• pp.77-82
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• 2002

It is well known that X-irradiation affects on maturing process of differentiated chondrocytes. Nevertheless, It has been remained elusively whether X-irradiation affects the process of differentiation of mesenchymal cells which differentiate into chondrocyte, fibroblast, or muscle cells. In this study, we examined the effect of X-irradiation (with 1 to 10 Gy) on chondrogenesis using the mesenchymal cells of chick limb bud. Our results show that X-irradiation dose-dependently inhibited chondrogenesis. This result suggests that immature chondroblast-like mesenchymal cells are sensitive to X-irradiation. Moreover, X-irradiation affects not only maturing process of chondrocytes, but also inhibits the chondrogenesis. Taken together, we demonstrate that the whole process of differentiation of mature chondrocytes from mesenchymal cells is affected by X-irradiation and undifferentiated cells were more affected by X-irradiation than mature cells.

• Korean Journal of Veterinary Service
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• v.28 no.4
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• pp.367-373
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• 2005

Coccidiosis of domestic fowl is a parasitic disease that infects poultry drastically and can cost the pastured poultry producer much in the course of a year. Two hundred forty, day-old-broiler chicks were purchased and were randomly divided in eight groups, containing thirty birds in each group. Decoquinate $6\%$, maduramicin ammonium $2\%$, monensin sodium $13.2\%$, salinomycin sodium $12\%$, a live attenuated vaccine, and trivalent live attenuated vaccine, was provided to the day chicks of six groups, respectively. The chicks of last two groups served as infected non-medicated and uninfected non-medicated, respectively. Feed consumption, weight gain, feed conversion ratio, mortality and oocyst count per gram feces were recorded during the conduction of the experiment. Among treated groups, performance of salinomycin group was significantly better (p<0.05) in all aspects. Salinomycin acts against the sporozoites, trophozoites and first generation schizonts and is highly effective against the economically important species of Eimeria. The present study confirms that use of salinomycin, as an anticoccidial, is a drug of choice.