• The Korean Journal of Physiology
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• v.19 no.2
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• pp.127-137
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• 1985

The present study was undertaken in order to investigate effect of ethanol extract of Rehmanniae radix(RREE) on electrophysiology of sinus node and papillary muscle. Rehmanniae radix is a herbal medicine which has been known to have diuretic, antipyretic, hemopoietic and cardiotonic effects. Action potentials were recorded by means of glass capillary microelectrode(technique) in rabbit sinoatrial nodal cells and papillary muscle cells which were superperfused with either tyrode solution or tyrode solutions containing different amount of RREE. The results obtained were as follows ; 1) In both central and peripheral nodal cells maximum diastolic potential (MDP) and amplitude of action potential (APA) were not affected by RREE. 2) Action potential duration as expressed $APD_{60}$(time to 60% repolarization) of central and peripheral pacemaker cells were significantly prolonged following perfusion with tyrode solution containing 0.1% RREE. 3) The rates of spontaneous firing from central pecemaker cell were decreased by RREE at concentration of 0.05% and 0. 1% while spontaneous rhythm of perinodal cell was decreased by 0.1% RREE. 4) The action potential duration of papillary muscle as expressed $APD_{60}$ were prolonged by 0.1% RREE.

• Biotechnology and Bioprocess Engineering:BBE
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• v.5 no.1
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• pp.44-47
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• 2000

Cell growth and DNA synthesis were studied from a cultured early- and late- pas- sage mouse aorta smooth muscle cell (MASMC) because the proliferation of vascular smooth muscle cell (VSMC) is a key factor in development of atherosclerosis. In this study, the cells were cultured in fetal bovine serum (FBS) and stimulated by growth factors such as thrombin and platelet-derived growth factor-BB (PDGF-BB). Compared to the number of early-passage MASMC (passage 3 to 9) the number of late-passage MASMC (passage 30 to 40) in a normal serum state was increased 2 fold at Day 1, 3 and 6 in culture, respectively. Incorporation of $[^3H]$ thymidine into DNA induced by serum, PDGF and thrombin in late-passage MASMC was greater than those in early-passage MASMC. We also examined whether intracellular zinc levels would be an aging factor or not. The intracellular zinc level in early- and late-passage MASMC was monitored by using the zinc probe dye N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide. It is interested that late-passage MASMC increased the intracellular fluorescence level of zinc, more than the early passage MASMC did. The alterations of intracellular zinc level occur concurrently with changes in MASMC proliferation rate during aging. This data suggest that the age-associated changes in zinc concentrations may provide a new in vitro model for the study of smooth muscle cell differentiation.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.12
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• pp.1751-1755
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• 2017

Objective: An experiment was conducted to study the blood haematology, muscle pH, and serum cortisol changes in pigs with different levels of drip loss. Methods: Two groups (low and high) of 20 animals were selected from 100 pigs based on drip loss. All [$Duroc{\times}(Large\;White{\times}Landrace)$] pigs were slaughtered according to standard slaughtering procedures. At exsanguinations, blood samples were taken for the haematological parameters and serum cortisol analysis. The muscle samples were taken from longissimus dorsi muscle to evaluate the muscle pH and drip loss. Results: Haematological parameters of low drip loss group showed higher content of white blood cells and monocytes than high drip loss group (p<0.05). The low drip loss group had higher muscle pH at 45 min (p<0.05) and 24 h (p<0.001) post-mortem than the high drip loss group. However, there was no significant difference in serum cortisol levels (p>0.05). Conclusion: Drip loss is mainly affected by the muscle pH decline after slaughter and also might be affected by white blood cells and monocytes.

• Archives of Pharmacal Research
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• v.23 no.6
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• pp.535-547
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• 2000

Recent findings indicate that mechanical strain (deformation) exerted by the extracellular matrix modulates activation of airway smooth muscle cells. Furthermore, cytoskeletal organization in airway smooth muscle appears to be dynamic, and subject to modulation by receptor activation and mechanical strain. Mechanosensitive modulation of crossbridge activation and cytoskeletal organization may represent intracellular feedback mechanisms that limit the shortening of airway smooth muscle during bronchoconstriction. Recent findings suggest that receptor-mediated signal transduction is the primary target of mechanosensitive modulation. Mechanical strain appears to regulate the number of functional G-proteins and/or phospholipase C enzymes in the cell membrane possibly by membrane trafficking and/or protein translocation. Dense plaques, membrane structures analogous to focal adhesions, appear to be the primary target of cytoskeletal regulation. Mechanical strain and receptor-binding appear to regulate the assembly and phosphorylation of dense plaque proteins in airway smooth muscle cells. Understanding these mechanisms may reveal new pharmacological targets for control1ing airway resistance in airway diseases.

• Journal of Life Science
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• v.27 no.8
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• pp.879-887
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• 2017

It is well established that brain-derived neurotrophic factor (BDNF) is expressed not only in the brain but also in skeletal muscle, and is required for normal neuromuscular system function. Histone deacetylases (HDACs) and insulin-like growth factor-I (IGF-I) are potent regulators of skeletal muscle myogenesis and muscle gene expression, but the mechanisms of HDAC and IGF-I in skeletal muscle-derived BDNF expression have not been examined. In this study, we examined the effect of IGF-I and suberoylanilide hydroxamic acid (SAHA), a pan-HDAC inhibitor, on BDNF induction. Proliferating or differentiating C2C12 skeletal muscle cells were treated with increasing concentrations (0-50 ng/ml) of IGF-I in the absence or presence of $5{\mu}M$ SAHA for various time periods (3-24 hr). Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent decrease in BDNF mRNA expression. However, inhibition of HDAC led to a significant increase in the expression of BDNF mRNA levels. In addition, immunocytochemistry revealed high BDNF protein levels in undifferentiated C2C12 skeletal muscle cells, whether untreated, IGF-I-treated, or exposed to SAHA. These results represent the first evidence that IGF-I can suppress the mRNA and protein expression of BDNF; conversely, SAHA attenuates the effects of IGF-I. Consequently, SAHA upregulates BDNF expression in C2C12 skeletal muscle cells.

• Animal cells and systems
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• v.5 no.3
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• pp.205-209
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• 2001

Mesenchymal cells from the leg buds of stage 24-chick embryos differentiated into chondrocytes when plated at high density. Treatment of high density micromass culture of chick mesenchymal cells with cytochalasin D(CD, 2 $\mu$M for 24 h) resulted in inhibition of chondrogenesis. CD treatment was found to affect the expression of the contractile protein $\alpha$-smooth muscle actin ($\alpha$-SM actin). In control cultures, $\alpha$-SM actin uniformly expressed from culture day 2, but the CD-treated cells induced expression of $\alpha$-SM actin from the first day of culture followed by a continuous increase. Expression of pan-cadherin (P-cadherin) decreased as chondrogenesis proceeded in the control culture, whereas the CD-treated cells showed sustained expression. These results propose a close connection of chondrogenic differentiation with expression of $\alpha$-SM actin and P-cadherin.

• Reproductive and Developmental Biology
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• v.30 no.1
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• pp.47-52
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• 2006

This study was conducted to examine whether the parthenogenetic mouse embryonic stem (P-mES) cells can differentiate into functional cardiomyocytes in vitro similar to (mES) cells. p-mES04 and IVF-derived mES03 cells were cultured by suspension culture for 4 days. The formed embryoid bodies (EBs) were treated with 0.75% dimethyl-sulfoxide (DMSO) for further 4 days (4-/4+), and then plated onto gelatin coated culture dish. The appearance of contracting cardiomyocytes from the P-mES04 and mES03 cells was examined for 30 days. The highest cumulative frequency was detected at days 13 (69.83%) and 22 (61.3%), respectively. By immunocytochemistry, beating P-mES04 cells were positively stained with muscle specific anti-sarcomeric a-actinin Ab and cardiac specific anti-cardiac troponin I Ab similar to contracted mES03 cells. When the expression of cardiac muscle-specific genes was analyzed by RT-PCR, beating P-mES04 cells were expressed cardiac specific L-type calcium channel, a1C, cardiac myosin heavy chain a, cardiac muscle heavy polypeptide $7{\beta}$, GATA binding protein 4 and atrial natriuretic factor, but not expressed skeletal muscle specific L-type calcium channel, a1S, which was similar to male adult heart cells and mES03-derived beating cardiomyocytes. The result demonstrates that the P-mES cells can be used as an alternative for the study on the characteristic analysis of in vitro cardiomyocyte differentiation from the ES cells.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.281-289
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• 1997

The study was designed to investigate the effects of progesterone and estrogen on the uterus of rats by immunohistochemical methods using Proliferating Cell Nuclear Antigen (PCNA) antibody. Eighteen female rats(Wistar), weighing initially about 300g, were ovariectomized. These rats were divided into four groups, progesterone-treated group, estrogen-treated group, estrogen+progesterone-treated group, and control group, progesterone-treated group was injected with 1mg of progesterone per rat per day for 2 days and estrogen-treated group with $20{\mu}g$ of $17{\beta}-estradiol$ for 3 days and estrogen+progesterone-treated group with $17{\beta}-estrdiol$ for 3 days and then with progesterone for 2 days as above. In gross findings, the uteri were markedly hypertrophied by estrogen treatment but were not affect in size by progesterone treatment. Immunohistochemical investigation was performed on the cell types with higher appearance of PCNA positive reaction cells in four groups. The groups with higher appearance of the stromal cells were ordered as estrogen-treated group, progesterone-treated group, estrogen+progesterone-treated group, and control group. The muscle cells were ordered as progesterone-treated group, estrogen-treated group, estrogen+progesterone-treated group, and control group. Positive reaction cells of the stromal cells were total 4.6 times higher than those of muscle cells. Therefore, the affect of the hypertrophy on the uterus by estrogen was larger than those of progesterone and affect on the uterus by stromal cells were larger than those of muscle cells. The group with more PCNA positive reaction cells of luminal epithelial cells were ordered as control group, progesterone-treated group, estrogen+progesterone-treated group, and estrogen-treated group, and glandular epithelial cells were ordered as estrogen+progesterone-treated group, progesterone-treated group, control group, and estrogen-treated group. It was suggested that estrogen and progesterone did not affect on the proliferating cells of luminal epithelial cells and affection of progesterone on the development of glandular epithelial cell was larger than that of estrogen.

• Journal of Microbiology and Biotechnology
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• v.34 no.2
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• pp.270-279
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• 2024

Macrophages are versatile immune cells that play crucial roles in tissue repair, immune defense, and the regulation of immune responses. In the context of skeletal muscle, they are vital for maintaining muscle homeostasis but macrophage-induced chronic inflammation can lead to muscle dysfunction, resulting in skeletal muscle atrophy characterized by reduced muscle mass and impaired insulin regulation and glucose uptake. Although the involvement of macrophage-secreted factors in inflammation-induced muscle atrophy is well-established, the precise intracellular signaling pathways and secretion factors affecting skeletal muscle homeostasis require further investigation. This study aimed to explore the regulation of macrophage-secreted factors and their impact on muscle atrophy and glucose metabolism. By employing RNA sequencing (RNA-seq) and proteome array, we uncovered that factors secreted by lipopolysaccharide (LPS)-stimulated macrophages upregulated markers of muscle atrophy and pro-inflammatory cytokines, while concurrently reducing glucose uptake in muscle cells. The RNA-seq analysis identified alterations in gene expression patterns associated with immune system pathways and nutrient metabolism. The utilization of gene ontology (GO) analysis and proteome array with macrophage-conditioned media revealed the involvement of macrophage-secreted cytokines and chemokines associated with muscle atrophy. These findings offer valuable insights into the regulatory mechanisms of macrophage-secreted factors and their contributions to muscle-related diseases.

• Clinical and Experimental Pediatrics
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• v.48 no.10
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• pp.1038-1049
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• 2005

Asthma is characterized by a chronic inflammatory disorder of the airways that leads to tissue injury and subsequent structural changes collectively called airway remodelling. Characteristic changes of airway remodelling in asthma include goblet cell hyperplasia, deposition of collagens in the basement membrane, increased number and size of microvessels, hypertrophy and hyperplasia of airway smooth muscle, and hypertrophy of submucosal glands. Apart from inflammatory cells, such as eosinophils, activated T cells, mast cells and macrophages, structural tissue cells such as epithelial cells, fibroblasts and smooth muscle cells can also play an important effector role through the release of a variety of mediators, cytokines, chemokines, and growth factors. Through a variety of inflammatory mediators, epithelial and mesenchymal cells cause persistence of the inflammatory infiltrate and induce airway structural remodelling. The end result of chronic airway inflammation and remodelling is an increased thickness of the airway wall, leading to a increased the bronchial hyperresponsiveness and fixed declined lung function.