- Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia.
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Byoung Yuk Yi, Sung Kyoo Hwang, Ku Seong Kang, Hong Hua Quan, Young Mi Lee, Jung Wan Kim, Eun Kyoung Kwak, Ji Young Park, Yoon Kyung Sohn
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Korean J Pathol. 2004;38(6):364-371.
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 Abstract
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- BACKGROUND
Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis.
METHODS
We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups.
RESULTS
TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased.
CONCLUSION
These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.
- Secretion of TNF-alpha via Proteinase-Activated Receptor-2 in Human Astrocyte Cell Line.
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Mi Sun Kim, Jin Ah Kim, Ok Hwa Kang, Ok Seon Baek, Jae Young Um, Jin Mu Yi, Ki Jung Yun, Hyung Min Kim, Young Mi Lee
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Korean J Pathol. 2003;37(3):159-165.
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Abstract
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- BACKGROUND
Proteinase-activated receptor 2 (PAR2) is cleaved, and it is activated by trypsin or mast cell tryptase. PAR2 plays an important role in inflammation. The aim of this study is to examine the potential of PAR2 agonists to modulate TNF-alpha secretion from the human astrocytoma cell line CCF-STTG1.
METHODS
PAR2 expression in CCF-STTG1 was examined using reverse transcriptase polymerase chain reaction and immunocytochemistry. The potential of PAR2 agonists to modulate TNF-alpha secretion from CCF-STTG1 was examined by enzyme-linked immunosorbent assays.
RESULTS
CCF-STTG1 expresses PAR2. PAR2 agonists such as trypsin, mast cell tryptase, and activating peptide SLIGKV-NH2 (corresponding to the PAR2 tethered ligand) directly signal CCF-STTG1 to induce the secretion of TNF-alpha but not in the case of the soybean trypsin inhibitor (SBTI) or VKGILS-NH2 (control peptide).
Furthermore, the secretion of TNF-alpha was significantly reduced in CCF-STTG1 cells pre-treated with either 50 microM PD98059 (mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) inhibitor) or 1 microM SB203580 (p38 MAPK inhibitor) 30 min before trypsin stimulation.
CONCLUSIONS
These results show that trypsin may induce TNF-alpha secretion through the activation of MEK and p38 MAPK via PAR2 in astrocytoma cell line CCF-STTG1.
- Immunocytochemical Characteristics of the Short-term cultured Mesothelial Cells.
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Ho Jong Jeon, Mi Ja Lee, Mi Sook Lee, Yu Kyung Jeong, Young Mi Lee, Hyung Ho Choi
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Korean J Cytopathol. 1995;6(2):106-115.
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Abstract
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- Reactive human mesothelial cells were examined by immunocytochemical stain with intermediate filaments(cytokeratin [CK1, CK7, CK8, CK18, CD19/, vimentin, desmin, actin), epithelial membrane antigen, carcinoembryonic antigen(CEA), MHC class II antigen(HLA-DR), LeuM-1(CD15), alpha1-antitrypsin(ACT), alpha1-antichymotrypsin (ACHT), CD68(KP-1) and FcgammaRIII(CD16). The mesothelial cells were isolated from patients with liver cirrhosis and pleural effusion, and short-term cultured in RPMI 1640 media containing 10% heat inactivated fetal calf serum and 1% identical supernatant fluid of the patients' transudates. The results obtained are as follows.
1. The cultured-reactive mesothelial cells were positive for the protein of cytoskeleton such as cytokeratin and vimentin, but negative for desmin and actin. The resting mesothelial cells showed positive reactions for cytokeratin, but negative for vimentin, desmin and actin.
2. The primary antibodies to the cytokeratin were strongly reactive for CK1, CK8 and CK18 but negative for CK7 and CK19 in both reactive and resting mesothelial cells.
3. Resting mesothelial cells showed negative reactions for CEA, but strong positive reactions in cultured-reactive mesothelial cells.
4. The markers for the monocytes\histiocytes (CD11b, CD14, CD16, CD68, lysozyme and alpha1-antitrypsin and alpha1-antichymotrypsin) were nonreactive in resting mesothelial cells, but lysozyme and alpha1-antitrypsin were weakly reactive in reactive and proliferative mesothelial cells.
5. MHC Class II molecule(HLA-DR antigen) was negative in both resting and reactive mesothelial cells.
These results suggest that the short-term cultured, reactive mesothelial cells show a newly aberrant expression of the vimentin and carcino-embryonic antigen. The reason of the aberrant expression of the intermediate filament and oncofetal antigen in reactive and proliferative mesothelial cells should be further evaluated.
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