• Journal of Microbiology and Biotechnology
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• v.19 no.5
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• pp.530-536
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• 2009

Cobalt chloride ($CoCl_2$) treatment of cells in vitro has been shown to induce cellular changes that are similar to those seen following hypoxia. To identify genes that are differentially expressed in response to treatment with $CoCl_2$, we compared the mRNA expression profiles of PC-3 cells that were treated with $CoCl_2$ with those of untreated PC-3 cells, using specific arbitrary primers and two anchored oligo(dT) primers provided in the ACP-based GeneFishing kits. The results of this study demonstrated that the puromycin-sensitive aminopeptidase (PSA) gene was down regulated in PC-3 cells that were treated with $CoCl_2$. This downregulation of PSA expression, in turn, suppressed the proliferation, migration, and invasion of PC-3 cells, as well as the secretion and expression of matrix metalloproteinase-9 (MMP-9).

• Journal of Life Science
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• v.21 no.2
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• pp.286-291
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• 2011

Hypoxia is a common condition found in a wide range of solid tumors and is often associated with metastasis and poor clinical outcomes. In the present study, we found that HIF-$1{\alpha}$ was induced by cobalt chloride (500 ${\mu}M$) treatment on human lung cancer cells, A549 and H460, for 24 hr. However, cobalt chloride (500 ${\mu}M$) did not affect cell proliferation of A549 and H460 in 48 hr. Cobalt chloride (500 ${\mu}M$) additionally induced epithelial-to-mesenchymal-like transition (EMT) such as reduced E-cadherin expression and increased ${\alpha}$-SMA expression. These results were confirmed by immunofluorecence experiment in H460 cells. E-cadherin was localized on the outer cell membrane. However, when the cells were treated with 500 ${\mu}M$ cobalt chloride for 24 hr, diffuse E-cadherin staining was observed, characteristic of a migratory mesenchymal phenotype. We also found that cobalt chloride induced integrin ${\beta}3$ expression and FAK phosphorylation in human lung cancer cells using western blotting and FACS anlaysis. Our data suggest that integrin ${\beta}3$-induced FAK phosphorylation may be developed into target molecules for blocking tumor metastasis.

• Journal of the Korean Chemical Society
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• v.47 no.4
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• pp.334-338
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• 2003

The crystal structure of $[Co(phen)_2(Cl)(H_2O)] Clㆍ2H_2O$(phen=1,10-phenanthroline) has been determined by X-ray crystallography. It crystallizes in the triclinic system, space group P1, with lattice parameters a=9.662(2), b=11.445(1), c=13.037(2)${\AA}$ ${\alpha}$=64.02(1), ${\beta}$=86.364(9), ${\gamma}=78.58(2)^°$, and Z=2. The coordinated cations contain a six-coordinated cobalt atom chelated by two phen ligands and one chloride anion and one water ligand in cis arrangement. In addition to the chloride coordinated to the cobalt, there are one chloride ion and four water molecules which complete the crystal structure. In the solid state, the title compound forms three dimensional network structure through hydrogen bonds, within which exists the strongest hydrogen bond (O(3)-O(4)=2.33${\AA}$). The intermolecular hydrogen bonds connect the $[Co(phen)_2(Cl)(H_2O)]1+,\;H_2O$ moieties and chloride ion.

• Bulletin of the Korean Chemical Society
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• v.18 no.4
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• pp.406-409
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• 1997

The various cobalt(Ⅱ) complexes were synthesized and characterized using tris-(2-benzimidazolylmethyl)amine (ntb) as a ligand where the ntb plays as a tripodal tetradentate ligand to form complexes with a trigonal pyramidal geometry. The complexes have 5 and 6 coordinate cobalt(Ⅱ) ions depending on the additional ligand used. In each complex the additional ligand, chloride anion, or acetate anion occupies the "open" site trans to the apical tertiary nitrogen atom of ntb ligand. Complex 1, [Co(Ⅱ)(ntb)Cl]Cl has a trigonal bipyramidal geometry. This geometry was easily constructed using ntb as a tetradentate ligand and chloride as a monodentate ligand. The complex is isostructural to the corresponding manganese(Ⅱ) complex. Crystal data are as follows: [Co(Ⅱ)(ntb)Cl]Cl·MeOH, 1. triclinic space group P1; a=13.524(2) Å, b=14.037(2) Å, c=17.275(1) Å; α=78.798(9), β=84.159(8)°, γ=65.504(9)°; V=2929.6(6) Å3; Z=4; R1=0.0715, wR2=0.1461 for reflections of I > 2σ(I). Six coordinate complex 2 [Co(ntb)(OAc)](OAc) was synthesized using ntb as a tetradentate ligand and acetate as a bidentate chelating ligand.

• Journal of Life Science
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• v.20 no.7
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• pp.991-998
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• 2010

Hypoxia is an indicative of pro-apoptotic and anti-apoptotic biphasic effects, which appear to be dependent upon the cell type and the condition of the cells. The hypoxia-mimetic agent, cobalt chloride ($CoCl_2$), has been shown to induce apoptosis in a variety of cell types, but the mechanism by which this occurs has yet to be thoroughly elucidated. Puromycin-sensitive aminopeptidase (PSA) gene was decreasingly expressed in response to $CoCl_2$. In this report, puromycin pretreatment applied to PC-3 cells resulted in apoptosis. To determine whether PSA is involved in apoptosis, we examined the apoptotic properties of the PC-3 cells after siRNA knockdown of PSA. PSA siRNA-induced PSA silencing revealed that endogenous PSA may be involved in apoptosis of the PC-3 cells. These results indicated that PSA may perform a vital function in cell survival of the PC-3 cells.

• IMMUNE NETWORK
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• v.13 no.4
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• pp.141-147
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• 2013

Hypoxia has been shown to promote inflammation, including the release of proinflammatory cytokines, but it is poorly investigated how hypoxia directly affects inflammasome signaling pathways. To explore whether hypoxic stress modulates inflammasome activity, we examined the effect of cobalt chloride ($CoCl_2$)-induced hypoxia on caspase-1 activation in primary mixed glial cultures of the neonatal mouse brain. Unexpectedly, hypoxia induced by oxygen-glucose deprivation or $CoCl_2$ treatment failed to activate caspase-1 in microglial BV-2 cells and primary mixed glial cultures. Of particular interest, $CoCl_2$-induced hypoxic condition considerably inhibited NLRP3-dependent caspase-1 activation in mixed glial cells, but not in bone marrow-derived macrophages. $CoCl_2$-mediated inhibition of NLRP3 inflammasome activity was also observed in the isolated brain microglial cells, but $CoCl_2$ did not affect poly dA:dT-triggered AIM2 inflammasome activity in mixed glial cells. Our results collectively demonstrate that $CoCl_2$-induced hypoxia may negatively regulate NLRP3 inflammasome signaling in brain glial cells, but its physiological significance remains to be determined.

• The Journal of the Convergence on Culture Technology
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• v.9 no.3
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• pp.587-592
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• 2023

Cobalt oxide (Co₃O₄·CoO) ultra fine particles were synthesized by liquid phase precursor method. cobalt(II) chloride hexahydrate (CoCl₂·6H₂O) was as a starting material. A plant-derived crystalline cellulose was used as impregnating materials. A impregnated precursor was calcined at a temperature of 350 to 900℃ to obtain cobalt oxide particles having a particle size of 1 to 10㎛. The crystallization process and morphology according to the calcination temperature were examined, and the properties of the synthesized powder were evaluated using SEM and XRD. It was confirmed that a crystal phase of Co₃O₄ began to form around 350℃ and crystal growth occurred up to 900℃. At a temperature above 500℃, the Co₃O₄ crystal was changed to another crystal phase CoO.

• Journal of the Korean Chemical Society
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• v.31 no.3
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• pp.231-235
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• 1987

In 10M chloride (4M HCl + 6M LiCl) solution, cobalt, but not nickel, formed complex anion (${CoCl_3}^-$), and this anion was extracted by a liquid anion exchanger with Amberlite LA-2. The ion exchange capacity was 2.175meq of cobalt complex per unit ml of Amberlite LA-2. Upon eluting the resin with 0.4M nitric acid, the cobalt complex was stripped and transfered into eluate quantitatively. By using this separation method in the chloride solution dissolved with 50mg of cobalt (II) and 500mg of nikel(II), recovery of cobalt were 99.6 percent.

• Journal of Life Science
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• v.23 no.11
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• pp.1342-1350
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• 2013

We examined the effect of hydrogen sulfide ($H_2S$) in chemical hypoxia-induced injury in mouse hepatocytes. Cell viability was significantly decreased by cobalt chloride ($CoCl_2$), a well-known hypoxia mimetic agent in a time- and dose- dependent manner. Sodium hydrosulfide (NaHS, a donor of $H_2S$) pretreatment before exposure to $CoCl_2$ significantly attenuated the $CoCl_2$-induced decrease of cell viability. $CoCl_2$ treatment resulted in an increase of intracellular ROS generation, which is inhibited by NaHS or N-acetyl-cysteine (NAC, a ROS scavenger), and p38 MAPK phosphorylation, which is also blocked by NaHS or NAC. The $CoCl_2$-induced increase of the Bax/Bcl-2 ratio was attenuated by NaHS, NAC, and SB 203580 (p38 MAPK inhibitor). The $CoCl_2$-induced decrease of cell viability was also attenuated by NaHS, NAC, and SB 203580 pretreatment. Additionally, NaHS inhibited the $CoCl_2$-induced COX-2. Similar to the effect of NaHS, NAC blocked $CoCl_2$-induced COX-2 expression. Furthermore, NS-398 (a selective COX-2 inhibitor) attenuated not only the $CoCl_2$-induced increase of the Bax/Bcl-2 ratio, it also decreased cell viability. Taken together, $H_2S$ protects primary cultured mouse hepatocytes against $CoCl_2$-induced cell injury through inhibition of the ROS-activated p38 MAPK cascade and the COX-2 pathway.

• Resources Recycling
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• v.11 no.6
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• pp.12-17
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• 2002

Solvent extraction experiments have been performed to separate copper from $CuCl_2$-$NiCl_2$-$CoCl_2$$ solutions using Alamine336 and LIX84. The complex formation tendency between metal ions and chloride ion had a great effect on the distribution coefficients of Cu, Co and Ni ions and separation factor of Cu to Co and Ni. In the experimental ranges of chloride ion concentration from 0.5 to 4.0 M, LIX84 was superior to Alamine336 in separating copper from cobalt. When the volume percentage of LIX84 and Alamine336 was varied from 5 to 40%, LIX84 was more effective than Alamine336 in separating Cu from Co and Ni in solutions in which the chloride ion concentration was 1.0 M.