• The Korean Journal of Zoology
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• v.39 no.1
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• pp.47-53
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• 1996

We examined the expression of the heat shock proteins (HSPs) and glucose-regulated proteins (GRPs) during phorbol 1 2-myristate 1 3-acetate (PMA)-induced megakaryocytic differentiation of human er"'throleukemia K562 cells. PMA-treated K562 cells showed a cell growth arrest and alteration in morphology and patterns of gpllIa and c-myc expression, characteristic of megakaryocytic differentiation. During the megakaryocytic differentiation, HSP9OA, HSP9OB, and HSP28 mRNA and protein levels markedly decreased, while GRP78/B and GRP94 mRNA levels were enhanced. On the other hand, HSP7OA and HSP7OB mRNA levels were reduced, but HSP7O protein levels were not changed by PMA treatment. These results suggest specific roles for the HSPs and GRPs in K562 cell proliferation and megakaryocic differentiation.tion.

• Journal of Applied Biological Chemistry
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• v.51 no.2
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• pp.50-56
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• 2008

As one way to approach to cold defense mechanism in plants, we previously identified the gene for protein-tyrosine phosphatase (CaTPP1) from hot pepper (Capsicum annuum) using cDNA microarray analysis coupled with Northern blot analysis. We showed that the CaTPP1 gene was strongly induced by cold, drought, salt and ABA stresses. The CaTPP1 gene was engineered under control of CaMV 35S promoter for constitutive expression in transgenic tobacco plants by Agrobacterium-mediated transformation. The resulting CaTPP1 transgenic tobacco plants showed significantly increased cold stress resistance. It also appeared that some of the transgenic tobacco plants showed increased drought tolerance. The CaTPP1 transgenic plants showed no visible phenotypic alteration compared to wild type plants. These results showed the involvement of protein tyrosine phosphatase in tolerance of abiotic stresses including cold and drought stress.

• Journal of Dental Rehabilitation and Applied Science
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• v.23 no.2
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• pp.179-186
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• 2007

The decrease of masticatory function caused by tooth loss leads to a decrease of cerebral blood flow volume resulting in impairment of cognitive function and learning memory disorder. However, the reduced mastication-mediated morphological alteration in the central nervous system (CNS) responsible for senile deficit of cognition, learning and memory has not been well documented. In this study, the effect of the loss of the molar teeth (molarless condition) on the hippocampal expression of glial fibrillary acidic protein (GFAP) protein was studied by immunohistochemical techniques. The results were as follows : 1. The molarless mice showed a lower density of pyramidal cells in the cornu ammonis 1 (CA1) and dentate gyrus (DG) region of the hippocampus than control mice. 2. Immunohistochemical analysis showed that the molarless condition enhanced the time-dependent increase in the cell density and hypertrophy of GFAP immunoreactivity in the CA1 region of the hippocampus. The molarless condition enhanced an time-dependent decrease in the number of neurons in the hippocampal formation and the time-dependent increase in the number and hypertrophy of GFAP-labeled cells in the same region. The data suggest a possible link between reduced mastication and histological changes in hippocampal formation that may be one risk factor for senile impairment of cognitive function and spatial learning memory.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.76-76
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• 2003

Mast cells accumulation can be causally related with several allergic inflammations. Previous work has demonstrated that glucocorticoids decreased tissue mast cell number and stem cell factor (SCF)-induced migration of mast cells required p38 mitogen-activated protein kinase (MAPK) activation. In the present study, we investigated the effects of dexamethasone on SCF-induced migration of rat peritoneal mast cells (RPMCs). SCF significantly induced migration of RPMCs at 4 h. Dexamethasone dose-dependently inhibited SCF-induced migration of RPMCs (about 90.1% at 100 nM, P<0.05). MAPK p38 inhibitor, SB203580 (20 ${\mu}$M) also inhibited the SCF-induced migration. The ability of SCF to enhance morphological alteration and F -actin formation was also abolished by treatment of dexamethasone. Dexamethasone inhibited SCF-induced p38 MAPK activation to near basal level and induced the MKP-1 expression. In addition, SCF-induced inflammatory cytokine production was significantly inhibited by treatment of dexamethasone or SB203580 (p<0.01). Our results show that dexamethasone potently regulates SCF -induced migration, p38 MAPK activation and inflammatory cytokine production through expression of MKP-l protein in RPMCs. Such modulation may have functional consequences during dexamethasone treatment, especially mast cell-mediated allergic inflammation disorders.

• BMB Reports
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• v.44 no.3
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• pp.176-181
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• 2011

Inhibiting histone deacetylase (HDAC) activity modulates the epigenetic status of cells, resulting in an alteration of gene expression and cellular function. Here, we investigated the effects of HDAC inhibitors on mouse embryonic stem (ES) cells. The HDAC inhibitors trichostatin A, suberoylanilide hydroxamic acid, sodium butyrate, and valproic acid induced early differentiation of mouse ES cells and triggered induction of heat-shock protein (HSP)70. In contrast, class III HDAC inhibitors failed to induce differentiation or HSP70 expression. Transcriptional upregulation of HSP70 was confirmed by mRNA expression analysis, an inhibitor study, and chromatin immunoprecipitation. HSP70 induction was dependent on the SAPK/JNK, p38, and PI3K/Akt pathways. Differentiation and induction of HSP70 by a subset of HDAC inhibitors was also examined in human ES cells, which suggests that the phenomenon generally occurs in ES cells. A better understanding of the effects of HDAC inhibitors may give more insight into their application in stem cell biology.

• Journal of Microbiology
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• v.40 no.3
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• pp.219-223
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• 2002

In order to investigate the function of Soo1p/${\alpha}$-COP during post-translational modification and intra-cellular transport of cell wall proteins in Saccharomyces cerevisiae, cell wall proteins from the soo1-1/ret1-1 mutant cells were analyzed. SDS-PAGE analysis of biotin labeled cell wall proteins suggested that the soo1-1 mutation impairs post-translational modification of cell wall proteins, such as N- and/ or Ο-glycosylation. Analysis of cell wall proteins with antibodies against ${\beta}$-1,3-glucan and ${\beta}$-1,6-glucan revealed alteration of the linkage between cell wall proteins and ${\beta}$-glucans in the soo1-1 mutant cells. Compositional sugar analysis of the cell wall proteins also suggested that the soo1-1 mutation impairs glycosylation of cell wall protein in the ER, which is crucial for the maintenance of cell wall integrity.

• Journal of Microbiology and Biotechnology
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• v.14 no.4
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• pp.836-843
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• 2004

Nontypeable H. influenzae (NTHi), a Gram-negative obligate human pathogen, causes pneumonia, chronic bronchitis, and otitis media, and the respiratory epithelium is the first line of defense that copes with the pathogen. In an effort to identify transcriptional responses of human respiratory epithelial cells to infection with NTHi, we examined its differential gene expression using high density cDNA microarrays. BEAS-2B human bronchial epithelial cells were exposed to NTHi for 3 hand 24 h, and the alteration of mRNA expression was analyzed using microarrays consisting of 8,170 human cDNA clones. The results indicated that approximately 2.6% of the genes present on the microarrays increased in expression over 2-fold and 3.8% of the genes decreased during the 24-h infection period. Upregulated genes included cytokines (granulocyte-macrophage colony stimulating factor 2, granulocyte chemotactic protein 2, IL-6, IL-10, IL-8), transcription factors (Kruppel-like factor 7, CCAAT/enhancer binding protein $\beta$, E2F-1, NF-$\kappa$B, cell surface molecules (CD74, ICAM-1, ICAM-2, HLA class I), as well as those involved in signal transduction and cellular transport. Selected genes were further confirmed by reverse-transcription-PCR. These data expand our knowledge of host cellular responses during NTHi infection and should provide a molecular basis for the study of host-NTHi interaction.

• Applied Microscopy
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• v.22 no.2
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• pp.127-140
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• 1992

This research was undertaken to determine the effects of the cyclophosphamide (CP) on the epididymal corpus of the male rat in terms of ultrastructural alteration and protein analysis by SDS-PAGE at different groups; control group, 1 week group, 3 weeks group and 5 weeks group were treated with saline (control group) or CP at doses of 20mg/kg/week, 1 time a week, respectively. In the cytoplasm of the principal cells on the epididymal corpus, the mitochondria were significantly swollen or disrupted. The lumens of rough endoplasmic reticulum (rER) were also dilated and the number of secretory vesicles and lysosomes were increased respectively. CP caused changes in protein concentrations in the corpus of epididymis after CP treatment. Total proteins of 31 to 36 species were expressed in the corpus fluid. Then the more CP was increased, the more concentration of proteins caused to decrease, synthesize or increase in epididymal corpus. In contrast to the control group, in particular 88KD and the other 8 proteins in the corpus fluid, were decreased or disappeared respectively, whereas acid phosphatase and the other 9 proteins in the corpus fluid, were increased or synthesized respectively. The other proteins are not showed distinctive difference. It is suggested that treatment with CP alters the specific cell organelles and proteins in segment of the epididymal corpus.

• Molecules and Cells
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• v.22 no.2
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• pp.220-227
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• 2006

Oxidative alteration of mitochondrial cytochrome c has been linked to disease and is one of the causes of proapoptotic events. We have investigated the modification of cytochrome c by $H_2O_2$. When cytochrome c was incubated with $H_2O_2$, oligomerization of the protein increased and the formation of carbonyl derivatives and dityrosine was stimulated. Radical scavengers prevented these effects suggesting that free radicals are implicated in the $H_2O_2$-mediated oligomerization. Oligomerization was significantly inhibited by the iron chelator, deferoxamine. During incubation of deoxyribose with cytochrome c and $H_2O_2$, damage to the deoxyribose occurred in parallel with the release of iron from cytochrome c. When cytochrome c that had been exposed to $H_2O_2$ was analyzed by amino acid analysis, the tyrosine, histidine and methionine residues proved to be particularly sensitive. These results suggest that $H_2O_2$-mediated cytochrome c oligomerization is due to oxidative damage resulting from free radicals generated by a combination of the peroxidase activity of cytochrome c and the Fenton reaction of free iron released from the oxidatively-damaged protein.

• YAKHAK HOEJI
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• v.36 no.5
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• pp.460-468
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• 1992

Several bichemical parameters related to free radicals were estimated in senile-prone (P) and resistant(R) strains of male senescence-accelerated mice(SAM) at 2, 5 and 11 months of age. The superoxide generation was increased with age in SAM-R/1 and SAM-P/2. Compared to SAM-R/1, more generation of superoxide was significantly noted in the SAM-P/2 liver. The activities of Cu/Zn-superoxide dismutase and catalase were decreased during aging and these activities in SAM-P/2 were significantly lower than in SAM-R/l liver. The activities of glutathione S-transferase were varied with aging, whereas SAM-P/2 showed lower levels compared to SAM-R/l. The gradual decreases of glutathione, protein bound-SH and nonprotein bound-SH contents were noted with increasing age. SAM-P/2 liver contained lesser amounts of glutathione and nonprotein bound-SH compared to SAM-R. In conclusion, superoxide generation was increased whereas the antioxidant enzyme activities were decreased during aging in SAM-R/1. In addition, SAM-P/2 strain showed more superoxide generation and less antioxidant enzyme activities than SAM-R/1 in the liver, thus we assume that these factors might accelerate the senescence of SAM-P/2 strain.