• Journal of Life Science
• /
• v.25 no.5
• /
• pp.585-593
• /
• 2015

Stress fiber (SF) alteration is mediated by cellular receptors, which, upon interaction with the extracellular counterpart, signal to the actin cytoskeleton for remodeling. This association is mediated by a variety of scaffold and signaling factors, which control the mechanical and signaling activities of the interaction site. The heterotrimeric transmembrane lymphotoxin α1β2 (LTα1β2), a member of the tumor necrosis factor (TNF) family of cytokines, including soluble homotrimeric lymphotoxin (LT α), plays an important role in lymphoid tissue architecture. Ligation between LTα1β2 and the lymphotoxin β receptor (LTβR) activates signal-cascade in fibroblastic reticular cells (FRCs). We found LTβR stimulation using an agonistic anti-LTβR antibody alone or combined with LTα or TNFα induced changes in the actin and plasticity of cells. To clarify the involvement of myosin underlying the alteration, we analyzed the effect of myosin light chain kinase (MLCK) with an MLCK inhibitor (ML7), the phosphorylation level of myosin light chains (MLC), and the level of phospho-myosin phosphatase target subunit 1 (MYPT1) after treatment with an agonistic anti-LTβR antibody for cytoskeleton reorganization in FRCs. The inhibition of MLCK activity induced changes in the actin cytoskeleton organization and cell morphology in FRC. In addition, we showed the phosphorylation of MLC and MYPT1 was reduced by LTβR stimulation in cells. A DNA chip revealed the LTβR stimulation of FRC down-regulated transcripts of myosin and actin components. Collectively, these results suggest LTβR stimulation is linked to myosin regarding SF alteration in FRC.

• The Korean Journal of Physiology and Pharmacology
• /
• v.14 no.5
• /
• pp.249-256
• /
• 2010

Gender differences in the trace elements of monkey sino-atrial (SA) node were investigated in a process of age-dependent alterations. Sixty hearts from Japanese and rhesus monkeys (30 male and 30 female) used were aged ranging from 1-day- to 30-year-old. The elements were analyzed using an inductively coupled plasma-atomic emission spectrometer (ICP-AES). Advancing age decreased all the trace elements. Ca, P, S and Mg significantly decreased. The correlation coefficients of Ca and P were $-0.178{\pm}0.081$ (p<0.05) and $-0.088{\pm}0.022$ (p<0.05) in male (n=30), and $-0.095{\pm}0.026$ (p<0.05) and $-0.069{\pm}0.017$ (p<0.05) in female (n=30), respectively. The age-dependent coefficients for Fe/Ca, Zn/Ca, Fe/P, Fe/S, Zn/S, Fe/Mg and Zn/Mg were exhibited markedly in male, but all was less in female. In gender-related differences, only a ratio of P/Ca (p<0.05) was significantly observed with ageing. The trace elements such as Cu, Se and Sn were less detected in the SA nodes. These results indicate that the age-dependent changes in the ratios of elements are appeared more rapidly in male monkey SA node, and the gender difference is observed in ratio of P/Ca. The different attenuations may be involved with the age- and gender-related SA nodal functions.

• Molecules and Cells
• /
• v.38 no.12
• /
• pp.1054-1063
• /
• 2015

Mitochondria play a crucial role in eukaryotic cells; the mitochondrial electron transport chain (ETC) generates adenosine triphosphate (ATP), which serves as an energy source for numerous critical cellular activities. However, the ETC also generates deleterious reactive oxygen species (ROS) as a natural byproduct of oxidative phosphorylation. ROS are considered the major cause of aging because they damage proteins, lipids, and DNA by oxidation. We analyzed the chronological life span, growth phenotype, mitochondrial membrane potential (MMP), and intracellular ATP and mitochondrial superoxide levels of 33 single ETC component-deleted strains during the chronological aging process. Among the ETC mutant strains, 14 ($sdh1{\Delta}$, $sdh2{\Delta}$, $sdh4{\Delta}$, $cor1{\Delta}$, $cyt1{\Delta}$, $qcr7{\Delta}$, $qcr8{\Delta}$, $rip1{\Delta}$, $cox6{\Delta}$, $cox7{\Delta}$, $cox9{\Delta}$, $atp4{\Delta}$, $atp7{\Delta}$, and $atp17{\Delta}$) showed a significantly shorter life span. The deleted genes encode important elements of the ETC components succinate dehydrogenase (complex II) and cytochrome c oxidase (complex IV), and some of the deletions lead to structural instability of the membrane-$F_1F_0$-ATP synthase due to mutations in the stator stalk (complex V). These short-lived strains generated higher superoxide levels and produced lower ATP levels without alteration of MMP. In summary, ETC mutations decreased the life span of yeast due to impaired mitochondrial efficiency.

• Journal of Microbiology and Biotechnology
• /
• v.22 no.7
• /
• pp.981-989
• /
• 2012

This study aimed to evaluate the effects of electroporation on the cell growth, cholesterol removal, and adherence abilities of L. acidophilus BT 1088 and their subsequent passages. The growth of electroporated parent cells increased (P<0.05) by 4.49-21.25% compared with that of the control. This may be attributed to the alteration of cellular membrane. However, growth of first, second, and third passages of treated cells was comparable with that of the control, which may be attributed to the resealing of transient pores on the cellular membrane. Electroporation also increased (P<0.05) assimilation of cholesterol by treated parent cells (>185.40%) and first passage (>21.72%) compared with that of the control. Meanwhile, incorporation of cholesterol into the cellular membrane was also increased (P<0.05) in the treated parent cells (>108.33%) and first passage (>26.67%), accompanied by increased ratio of cholesterol:phospholipids (C:P) in these passages. Such increased ratio was also supported by increased enrichment of cholesterol in the hydrophilic heads, hydrophobic tails, and the interface regions of the membrane phospholipids of both parent and first passage cells compared with that of the control. However, such traits were not inherited by the subsequent second and third passages. Parent cells also showed decreased intestinal adherence ability (P<0.05; decreased by 1.45%) compared with that of the control, without inheritance by subsequent passages of treated cells. Our data suggest that electoporation could be a potential physical treatment to enhance the cholesterol removal ability of lactobacilli that was inherited by the first passage of treated cells without affecting their intestinal adherence ability.

• International Journal of Oral Biology
• /
• v.45 no.4
• /
• pp.190-196
• /
• 2020

Several factors, including genetic and environmental insults, impede protein folding and secretion in the endoplasmic reticulum (ER). Accumulation of unfolded or mis-folded protein in the ER manifests as ER stress. To cope with this morbid condition of the ER, recent data has suggested that the intracellular event of an unfolded protein response plays a critical role in managing the secretory load and maintaining proteostasis in the ER. Tauroursodeoxycholic acid (TUDCA) is a chemical chaperone and hydrophilic bile acid that is known to inhibit apoptosis by attenuating ER stress. Numerous studies have revealed that TUDCA affects hepatic diseases, obesity, and inflammatory illnesses. Recently, molecular regulation of ER stress in tooth development, especially during the secretory stage, has been studied. Therefore, in this study, we examined the developmental role of ER stress regulation in tooth morphogenesis using in vitro organ cultivation methods with a chemical chaperone treatment, TUDCA. Altered cellular events including proliferation, apoptosis, and dentinogenesis were examined using immunostaining and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. In addition, altered localization patterns of the formation of hard tissue matrices related to molecules, including amelogenin and nestin, were examined to assess their morphological changes. Based on our findings, modulating the role of the chemical chaperone TUDCA in tooth morphogenesis, especially through the modulation of cellular proliferation and apoptosis, could be applied as a supporting data for tooth regeneration for future studies.

• Molecules and Cells
• /
• v.37 no.10
• /
• pp.713-718
• /
• 2014

Alteration in chromosome numbers and structures instigate and foster massive genetic instability. As Boveri has seen a hundred years ago (Boveri, 1914; 2008), aneuploidy is hall-mark of many cancers. However, whether aneuploidy is the cause or the result of cancer is still at debate. The molecular mechanism behind aneuploidy includes the chromosome mis-segregation in mitosis by the compromise of spindle assembly checkpoint (SAC). SAC is an elaborate network of proteins, which monitor that all chromosomes are bipolarly attached with the spindles. Therefore, the weakening of the SAC is the major reason for chromosome number instability, while complete compromise of SAC results in detrimental death, exemplified in natural abortion in embryonic stage. Here, I will review on the recent progress on the understanding of chromosome missegregation and cancer, based on the comparison of different mouse models of BubR1, the core component of SAC.

• Biomolecules & Therapeutics
• /
• v.23 no.3
• /
• pp.290-295
• /
• 2015

Aging is defined as a collective process that alters organism's functional capacity and appearance over the course of life. Apart from an increase in susceptibility to many diseases, aging affects the cellular system that is responsible for decoding painful stimuli. Yet, aging-associated molecular mechanisms of pain perception remains elusive. Using Drosophila, we showed a decrease in temperature tolerance and a reduction in high temperature thermal avoidance with aging. Locomotor activity assay demonstrated that the age-dependent changes in heat nociception did not stem from the general decline in muscular activity. However, we identified pain-related gene expression alteration with aging. We anticipate that our findings would help opening a new window onto developing the optimal pain treatment for the elderly.

• The Journal of the Korean dental association
• /
• v.48 no.8
• /
• pp.576-586
• /
• 2010

Recent advancement in molocular biology enhanced further understanding of the carcinogenesis of oral cancer and its relation with various genetic backgrounds. Familial risk factors includes similar habits of the family and polymorphic variations of the genes. Recently, human papilloma virus has been suggested to be linked with oral cancer progression. Enhancement of understanding of the damage or alteration in molecular pathway in various cellular response of oral cancer progression would lead the targeted therapy or precise early diagnosis of the oral cancer.

• BMB Reports
• /
• v.45 no.11
• /
• pp.604-611
• /
• 2012

Recent advances in genome and transcriptome analysis have enabled identification of numerous members of a new class of noncoding RNA, long noncoding RNA (lncRNA). lncRNAs are broadly defined as RNA molecules greater than 200 nt in length and lacking an open reading frame. Recent studies provide evidence that lncRNAs play central roles in a wide range of cellular processes through interaction with key component proteins in the gene regulatory system, and that alteration of their cell- or tissue-specific expression and/or their primary or secondary structures is thought to promote cell proliferation, invasion and metastasis. The biological and molecular characteristics of the large majority of lncRNAs remains unknown, and it is anticipated that improved understanding of the roles played by lncRNAs in cancer will lead to the development of novel biomarkers and effective therapeutic strategies.

• BMB Reports
• /
• v.42 no.6
• /
• pp.324-330
• /
• 2009

Autophagy is a bulk lysosomal degradation process important in development, differentiation and cellular homeostasis in multiple organs. Interestingly, neuronal survival is highly dependent on autophagy due to its post-mitotic nature, polarized morphology and active protein trafficking. A growing body of evidence now suggests that alteration or dysfunction of autophagy causes accumulation of abnormal proteins and/or damaged organelles, thereby leading to neurodegenerative disease. Although autophagy generally prevents neuronal cell death, it plays a protective or detrimental role in neurodegenerative disease depending on the environment. In this review, the two sides of autophagy will be discussed in the context of several neurodegenerative diseases.