• Applied Microscopy
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• v.36 no.1
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• pp.25-33
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• 2006

This study applied a bleaching agent. which is commonly used in the beauty salons, to the hair of normal adult women, collected the hair immediately and 10 days and 20 days from the bleaching, were investigated the degree of degradation of the hair by using scanning and transmission electron microscopes. The surface of hair just after bleaching was observed to be similar to that of normal hair, showing no split or damage of scale. In the hair of 10 days after bleaching, however, the scale came off. From this time, scale on the cuticular layer of hair began to be separated. In 10 days from bleaching, the scale on the cuticular layer was separated from hair and some cytoplasm of cuticular cells was broken into pieces or fell off. The cell remains made the surface coarse and uneven. At this period, damaged scales had a sharp end. In the hair of 20 days after bleaching, scale fell off from the whole surface of the hair and the surface looked rough. On the bleached hair, many vacuoles were formed in the endocuticle of cuticular cells. As a result, deformation caused by the formation of vacuoles in cuticles broke up the cuticular cells.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.5
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• pp.225-230
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• 2008

Netrins are secreted molecules and involved in axon guidance, cell migration and tumor development. Recent studies revealed that netrins perform novel functions in such processes as epithelial development and angiogenesis without operating through the classical netrin receptors, DCC (Deleted in Colorectal Cancer) and Unc5h. In the present study, we investigated the roles of netrin-1 and its receptors in cell spreading of human glioblastoma cells, and found that netrin-1 haptotactically enhanced fibronectin-induced cell spreading and focal adhesion formation in U373 glioblastoma cells. Netrin-1 binding to the U373 cell membrane was blocked by an antibody against ${\alpha}v$ integrin subunit, but not by an anti-DCC or anti-Unc5h antibody. In addition, enhancement of the fibronectin response by netrin-1 was abrogated by a function blocking antibody against integrin ${\alpha}v{\beta}3$. Since the ${\alpha}v$ subunit of the integrin family plays an important role in the pathophysiological aspects of cell migration, including tumor angiogenesis and metastasis, our data provide important insight into the molecular mechanism of netrin function.

• Journal of the Korean Magnetic Resonance Society
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• v.21 no.2
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• pp.72-77
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• 2017

${\beta}-catenin$ is a key signaling protein which regulates cell signaling and gene transcription. Abnormal activation of ${\beta}-catenin$ is linked to many cancers, particularly with colorectal cancers. Although many genetic and biological studies on $Wnt/{\beta}-catenin$ have been reported and structures of the complex between ${\beta}-catenin$ and its diverse binding partners have been published, many of them have focused on armadillo repeat domain of ${\beta}-catenin$. Both N- and C-terminal domains have been suggested to regulate interactions of ${\beta}-catenin$ with other molecules, but still little is known about the C-terminal unstructured domain. To investigate the structure of this domain, construct of C-terminus was designed and structural studies were performed using size exclusion chromatography (SEC), circular dichroism (CD), fluorescence and nuclear magnetic resonance (NMR) spectroscopy. We observed that not only the purified full-length construct but the purified C-terminal construct also dimerizes in solution by SEC, suggesting that this domain involves in dimerization of ${\beta}-catenin$. CD and fluorescence data indicate its flexibility and structural formation in the presence of membrane environments.

• Korean Journal of Pharmacognosy
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• v.43 no.1
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• pp.72-78
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• 2012

Alnus japonica Steud (A. japonica) have long been used in the traditional medicine for gastric disorder, hepatitis and fatty liver in Korea. Antiulcer effects of A. japonica hot water extract (AJ ext) were evaluated by in vitro antibacterial activity against H. pylori, by the inhibitory action against the in vitro gastric $H^+/K^+$-ATPase and using rat models of gastric mucosal damage and gastric ulcer induced by HCl-ethanol, indomethacin, and restraint and water-immersion stress. For the determination of antibacterial activity of AJ ext against H. pylori, the activity of urease which released from H. pylori was measured in culture. AJ ext showed weak antibacterial activity against H. pylori with the growth inhibitions of 37% and 61% by adding final concentrations of 500 and $1000{\mu}g/ml$ culture, respectively at 24 h. To observe the inhibitory activity of AJ ext against the $H^+/K^+$-ATPase in hog gastric membrane vesicle, $IC_{50}$ value of AJ ext was $806.3{\mu}g/ml$. Pretreatment of AJ ext (200, 500 mg/kg, p.o.) prevented in a dose-dependent manner the acute gastritis in HCl-ethanol model and the formation of gastric ulcer in indomethacin model and restraint and water-immersion stress model. These results suggest that the AJ ext can be used for prevention and treatment of gastric mucosal damage and ulcers induced by various stress.

• Korean Journal of Veterinary Research
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• v.35 no.3
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• pp.563-573
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• 1995

To know the effect of Ivermectin(IVM) toxicity in testis, histopathologic changes as well as clinical signs were observed in experimental animals including dogs by the subcutaneous injection with 3-50mg/kg of IVM. Clinically, it was observed to have depression and ataxia in all groups whereas tremor and coma in mice, rats and guinea pigs, coma in hamsters and rabbits, and tremor and salivation in dogs were shown. The clinical signs were different by the dosage of IVM, species and individuals in all animals. Susceptibility to IVM was most sensitive in dogs, especially in a Tosa dog and this was susceptible in mice, hamsters and rabbits, guinea pigs and rats in order. Microscopical observation revealed that the seminiferous tubules of testis had decreased thickness of germinal epithelium due to the necrosis and desquamation of the spermatids and spermatocytes. The progressive pattern by the times of administration showed vacuolar formation between the layer of spermatids and spermatogonia due to the marked necrosis of spermatocytes and the presence of multinucleated giant cells derived from spermatid throughout the seminiferous tubules of testis. Only a layer of spermatogonia, a few spermatogonia, and Sertoli cells wore observed with atrophied wavelike basement membrane in the seminiferous tubules of testis. Necrotic germinal cells, sloughed immature spermatids and spermatocytes were present in the lumen of epididymis and ductus deferens. Microscopical observation showed different susceptibility to IVM with clinical observation in which it was also most sensitive in dogs, especially in a Tosa dog and this was susceptible in rabbits and guinea pigs, hamsters, rats and mice in order. It was considered that IVM affects mainly spermatocyte or spermatid stage in the spermatogenesis and disturbs their developing beyond these stage.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.3
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• pp.709-713
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• 2007

Basement membranes (BMs) are extracellular matrices associated with epithelia, endothelia, muscle, fat and peripheral nerve. They are involved in cell survival, migration, differentiation. BMs functions also include tissue formation and provide mechanical stability as a selective barriers. Laminins are heterotrimeric glycoproteins found in BMs and have a crucial role in cell adhesion and signalling. Madin-Darby canine kidney (MDCK) cells are the best established mammalian model for studying epithelial cell biology The cells form an epithelial monolayer, with tight junctions separating an apical surface from a basolateral membrane facing the filter support and neighboring cells. In this study, using MDCK cells, the synthesis of the BM protein such as laminin with or without methanol extract of Chrysanthemum morifolium (CM) stimulation was analyzed by immunoblotting and CM showed significant increased cell density and enhanced synthesis of laminin.

• Molecules and Cells
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• v.43 no.9
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• pp.821-830
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• 2020

Altered dendritic morphology is frequently observed in various neurological disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the cellular and molecular basis underlying these pathogenic dendritic abnormalities remains largely unclear. In this study, we investigated dendritic morphological defects caused by dipeptide repeat protein (DPR) toxicity associated with G4C2 expansion mutation of C9orf72 (the leading genetic cause of ALS and FTD) in Drosophila neurons and characterized the underlying pathogenic mechanisms. Among the five DPRs produced by repeat-associated non-ATG translation of G4C2 repeats, we found that arginine-rich DPRs (PR and GR) led to the most significant reduction in dendritic branches and plasma membrane (PM) supply in Class IV dendritic arborization (C4 da) neurons. Furthermore, expression of PR and GR reduced the number of Golgi outposts (GOPs) in dendrites. In Drosophila brains, expression of PR, but not GR, led to a significant reduction in the mRNA level of CrebA, a transcription factor regulating the formation of GOPs. Overexpressing CrebA in PR-expressing C4 da neurons mitigated PM supply defects and restored the number of GOPs, but the number of dendritic branches remained unchanged, suggesting that other molecules besides CrebA may be involved in dendritic branching. Taken together, our results provide valuable insight into the understanding of dendritic pathology associated with C9-ALS/FTD.

• Bulletin of the Korean Chemical Society
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• v.20 no.9
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• pp.1078-1084
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• 1999

A synthetic cecropin A(1-13)-melittin(1-13) [CA-ME] hybrid peptide was known to be an antimicrobial peptide having strong antibacterial, antifungal and antitumor activity with minimal cytotoxic effect against human erythrocyte. Analogues were synthesized to investigate the influences of the flexible hinge region of CA-ME on the antibiotic activity. Antibiotic activity of the peptides was measured by the growth inhibition against bac-terial, fungal and tumor cells and vesicle-aggregating or disrupting activity. The deletion of Gln-Gly-Ile (P1) or Gly-Gln-Gly-Ile-Gly (P3) from CA-ME brought about a significant decrease on the antibiotic activities. In contrast, Gly-Ile-Gly deletion (P2) from CA-ME or Pro insertion (P5) instead of Gly-Gln-Gly-Ile-Gly of CA-ME retained antibiotic activity. This result indicated that the flexible hinge or β-bend structure provided by Gly-Gln-Gly-Ile-Gly, Gln-Gly, or Pro in the central region of the peptides is requisite for its effective antibiotic activity and may facilitate easily the hydrophobic C-terminal region of the peptide to penetrate the lipid bilayers of the target cell membrane. In contrast, P4 and P6 with Gly-Gln-Gly-Pro-Gly or Gly-Gln-Pro in the central region of the peptide caused a drastic reduction on the antibiotic activities. This result suggested that the con-secutive β-bend structure provided by Gly-Gln-Gly-Pro-Gly or Gly-Gln-Pro in the central hinge region of the peptide seems to interrupt the ion channel/pore formation on the target cell membranes.

• Biomolecules & Therapeutics
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• v.27 no.6
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• pp.530-539
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• 2019

Brain aging is an inevitable process characterized by structural and functional changes and is a major risk factor for neurodegenerative diseases. Most brain aging studies are focused on neurons and less on astrocytes which are the most abundant cells in the brain known to be in charge of various functions including the maintenance of brain physical formation, ion homeostasis, and secretion of various extracellular matrix proteins. Altered mitochondrial dynamics, defective mitophagy or mitochondrial damages are causative factors of mitochondrial dysfunction, which is linked to age-related disorders. Etoposide is an anti-cancer reagent which can induce DNA stress and cellular senescence of cancer cell lines. In this study, we investigated whether etoposide induces senescence and functional alterations in cultured rat astrocytes. Senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity was used as a cellular senescence marker. The results indicated that etoposide-treated astrocytes showed cellular senescence phenotypes including increased SA-${\beta}$-gal-positive cells number, increased nuclear size and increased senescence-associated secretory phenotypes (SASP) such as IL-6. We also observed a decreased expression of cell cycle markers, including PhosphoHistone H3/Histone H3 and CDK2, and dysregulation of cellular functions based on wound-healing, neuronal protection, and phagocytosis assays. Finally, mitochondrial dysfunction was noted through the determination of mitochondrial membrane potential using tetramethylrhodamine methyl ester (TMRM) and the measurement of mitochondrial oxygen consumption rate (OCR). These data suggest that etoposide can induce cellular senescence and mitochondrial dysfunction in astrocytes which may have implications in brain aging and neurodegenerative conditions.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.6
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• pp.539-547
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• 2019

Anoctamin 5 (ANO5)/TMEM16E belongs to a member of the ANO/TMEM16 family member of anion channels. However, it is a matter of debate whether ANO5 functions as a genuine plasma membrane chloride channel. It has been recognized that mutations in the ANO5 gene cause many skeletal muscle diseases such as limb girdle muscular dystrophy type 2L (LGMD2L) and Miyoshi muscular dystrophy type 3 (MMD3) in human. However, the molecular mechanisms of the skeletal myopathies caused by ANO5 defects are poorly understood. To understand the role of ANO5 in skeletal muscle development and function, we silenced the ANO5 gene in C2C12 myoblasts and evaluated whether it impairs myogenesis and myotube function. ANO5 knockdown (ANO5-KD) by shRNA resulted in clustered or aggregated nuclei at the body of myotubes without affecting differentiation or myotube formation. Nuclear positioning defect of ANO5-KD myotubes was accompanied with reduced expression of Kif5b protein, a kinesin-related motor protein that controls nuclear transport during myogenesis. ANO5-KD impaired depolarization-induced $[Ca2^{+}]_i$ transient and reduced sarcoplasmic reticulum (SR) $Ca^{2+}$ storage. ANO5-KD resulted in reduced protein expression of the dihydropyridine receptor (DHPR) and SR $Ca^{2+}-ATPase$ subtype 1. In addition, ANO5-KD compromised co-localization between DHPR and ryanodine receptor subtype 1. It is concluded that ANO5-KD causes nuclear positioning defect by reduction of Kif5b expression, and compromises $Ca^{2+}$ signaling by downregulating the expression of DHPR and SERCA proteins.