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- 저자 : Okjoon KIM (검색결과 18 건)
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Immunohistochemical Study of Nitric Oxide Synthase in Pleomorphic Adenoma of the Salivary Glands
김옥준(Okjoon Kim),김도균(Dogyun Kim),정지연(Ji Yeun Jeong),김현진(Hyun Jin Kim),김원재(Won Jae Kim),최홍란(Hongran Choi),김선헌(Sunhun Kim) 대한해부학회 2003 Anatomy & Cell Biology Vol.36 No.2
산화질소는 신생혈관생성, 암종의 전이등 종양에 영향을 미치는 것으로 알려져 있으나, 머리 및 목에서 발생하는 종양 에 대한 산화질소 활성도에 관한 연구는 거의 없다. 본 연구는 침샘에서 발생하는 양성 종양 중 가장 빈번한 다형성 선종 및 인접 정상조직에서 eNOS (산화질소합성효소) 및 iNOS의 발현도를 알아보기 위해 면역조직화학검사를 시행하였다. 면역조직화학검사 결과 다형성 선종에서 인접 정상조직보다 높은 NOS의 발현을 보였는데, 이는 산화질소합성효소의 증가가 종양 생성 및 진행과 관련성이 있음을 시사한다. 또한, NOS 발현은 간엽성 유래 구성요소 보다는 상피성 유래 구성요소에서 더 높게 발현되었다. 대체로 다형성 선종에서는 iNOS의 발현이 eNOS보다 높게 나타났다. 다형성 선종에 인접한 정상조직에서 iNOS의 발현은 간엽성이 우세한 것보다 상피성이 우세한 다형성 선종에서 더 높게 발현되어 eNOS보다는 iNOS 가 종양의 진행에 더 관여할 것으로 추측된다. 결론적으로 산화질소는 종양의 초기성장과 진행에 있어 중요한 인자이며, 앞으로 종양 성장에 중요한 인자인 신생혈관생성에 관련한 인자와 함께 더 많은 연구가 필요할 것으로 사료된다. Recent studies have suggested that nitric oxide (NO) exerts various effects on aspects of tumor biology, including angiogenesis and metastasis. There have been, however, scanty reports on nitric oxide synthase (NOS) response for tumors of the head and neck. This study was carried out to assess the distribution of both endothelial NOS (eNOS) and inducible NOS (iNOS) in normal salivary gland tissue and in pleomorphic adenoma by using immunohistochemistry. In the present study, eNOS and iNOS were higher expressed in pleomorphic adenoma than adjacent normal salivary gland tissue, suggesting that up-regulation of this enzyme is associated with tumor progression. Additionally, eNOS and iNOS expression were higher in epithelial components than in mesenchymal components. Overall, iNOS expression was higher than eNOS expression in pleomorphic adenoma. In normal tissues adjacent to pleomorphic adenoma, iNOS expression was higher in the mesenchymal type than in the epithelial type of pleomorphic adenoma. It is suggested that NO may play a role in the tumorgenesis and propagation of pleomorphic adenoma.
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KIM, JISUN,LIM, HAESOON,KIM, SANGWOO,CHO, HYEJUNG,KIM, YONG,LI, XIAOJIE,CHOI, HONGRAN,KIM, OKJOON Spandidos Publications 2016 Oncology Reports Vol.35 No.4
<P>We previously reported that photodynamic therapy (PDT) induces cell death in head and neck cancer through both autophagy and apoptosis. Regulation of cell death by autophagy and apoptosis is important to enhance the effects of PDT. Autophagy maintains a balance between cell death and PDT resistance. Downregulation of heat shock protein 27 (HSP27) induces PDT resistance in head and neck cancer cells. Furthermore, HSP70 regulates apoptosis during oxidative stress. However, the role of HSPs in PDT-induced cell death through autophagy and apoptosis is unclear. Therefore, in the present study, we investigated the effects of HSP27 and HSP70 on PDT-induced cell death of oral cancer cells through autophagy and apoptosis. Cancer cells were treated with hematoporphyrin at varying doses, followed by irradiation at 635 nm with an energy density of 5 mW/cm(2). We determined the changes in HSP expression by determining the levels of PARP-1 and LC3II in PDT-resistant cells. Furthermore, we assessed cell death signaling after downregulating HSPs by transfecting specific siRNAs. We observed that PDT decreased HSP27 expression but increased HSP70 expression in the head and neck cancer cells. Treatment of cells with LC3II and PARP-1 inhibitors resulted in upregulation of HSP70 and HSP27 expression, respectively. Downregulation of HSP27 and HSP70 induced cell death and PDT resistance through autophagy and apoptosis. Moreover, downregulation of HSP27 in PDT-resistant cells resulted in enhanced survival. These results indicate that the regulation of HSP27 and HSP70 plays a principal role in increasing the effects of PDT by inducing autophagic and apoptotic cell death.</P>
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Kim, Hyunju,Shin, Min-Ho,Yoon, Suk-Ja,Kweon, Sun-Seog,Lee, Young-Hoon,Choi, Chang-Kyun,Kim, OkJoon,Kim, Young-Joon,Chung, HyunJu,Kim, Ok-Su Korean Academy of Periodontology 2020 Journal of Periodontal & Implant Science Vol.50 No.6
Purpose: Vitamin D deficiency may cause bone loss and increased inflammation, which are well-known symptoms of periodontal disease. This study investigated whether serum 25-hydroxyvitamin D (25(OH)D) levels are associated with periodontal disease status and tooth loss. Methods: Cross-sectional data from 5,405 individuals aged ≥50 years (2,253 males and 3,152 females) were obtained from the 2008-2010 Dong-gu study, a prospective cohort study of risk factors for chronic diseases. Periodontal examinations were conducted to evaluate the number of remaining teeth, the periodontal probing depth (PPD), the clinical attachment level (CAL), and bleeding on probing. The percentages of sites with PPD ≥4 mm and CAL ≥4 mm were recorded for each participant. The severity of periodontitis was classified using the Centers for Disease Control and Prevention and the American Academy of Periodontology case definitions. Serum 25(OH)D levels were classified as reflecting severe deficiency, deficiency, insufficiency, or sufficiency. Multivariate linear regression analysis was performed to assess the associations of serum 25(OH)D levels with periodontal parameters and the number of remaining teeth after adjusting for confounders including age, smoking status, alcohol consumption status, month of blood collection, and physical activity. Multivariate logistic regression was used to evaluate the association between serum vitamin D levels and severe periodontitis. An overall statistical analysis and a stratified analysis by sex were performed. Results: Overall, the rates of severe deficiency, deficiency, insufficiency, and sufficiency were 6.5%, 67.9%, 22.4%, and 3.2%, respectively. After adjustment for confounders, vitamin D levels were directly associated with the number of remaining teeth, an association that was significant in males, but not in females. Sufficient serum 25(OH)D was associated with a low frequency of severe periodontitis. Conclusions: This population-based cross-sectional study indicates that low serum 25(OH) D is significantly associated with tooth loss and severe periodontitis in Koreans aged 50 years and older.
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Choi, HongRan,Lim, WonBong,Kim, InAe,Kim, JiSun,Ko, YoungJong,Kwon, Hyukil,Kim, SangWoo,Kabir, K M Ahsan,Li, Xiaojie,Kim, Oksu,Lee, YoungJoon,Kim, SeoYune,Kim, OkJoon Baillière Tindall ; Springer London 2012 LASERS IN MEDICAL SCIENCE Vol.27 No.2
<P>Human gingival fibroblasts (hGFs) play an important role in the inflammatory reaction to lipopolysaccharide (LPS) from P. gingivalis, which infects periodontal connective tissue. In addition, although light-emitting diode (LED) irradiation has been reported to have biostimulatory effects, including anti-inflammatory activity, the pathological mechanisms of these effects are unclear. This study examined the effects of 635-nm irradiation of P. gingivalis LPS-treated human gingival fibroblasts on inflammatory cytokine profiles and the mitogen-activated protein kinase (MAPK) pathway, which is involved in cytokine production. Gingival fibroblasts treated or not treated with P. gingivalis LPS were irradiated with 635-nm LED light, and cytokine profiles in the supernatant were assessed using a human inflammation antibody array. Expression of cyclooxyginase-2 (COX-2) protein and phosphorylation of extracellular signal-regulated kinase (ERK 1/2), p38, and c-Jun-N-terminal kinase (JNK) were assessed by Western-blot analysis to determine the effects on the MAPK pathway, and prostaglandin E(2) (PGE(2)) in the supernatant was measured using an enzyme-linked immunoassay. COX-2 protein expression and PGE(2) production were significantly increased in the LPS-treated group and decreased by LED irradiation. LPS treatment of gingival fibroblasts led to the increased release of the pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8, whereas LED irradiation inhibited their release. Analysis of MAPK signal transduction revealed a considerable decrease in p38 phosphorylation in response to 635-nm radiation either in the presence or absence of LPS. In addition, 635-nm LED irradiation significantly promoted JNK phosphorylation in the presence of LPS. LED irradiation can inhibit activation of pro-inflammatory cytokines, mediate the MAPK signaling pathway, and may be clinically useful as an anti-inflammatory tool.</P>
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Cell Death and Intracellular Distribution of Hematoporphyrin in a KB Cell Line
Choi, Hongran,Lim, Wonbong,Kim, Ji-Eun,Kim, Inae,Jeong, Jinan,Ko, Youngjong,Song, Jongwoon,You, Sunyeol,Kim, Doman,Kim, Misook,Kim, Byung-Kuk,Kim, Okjoon Mary Ann Liebert 2009 Photomedicine and laser surgery Vol.27 No.3
<P>OBJECTIVE: The objective of this study is to investigate the effect of intracellular photosensitizer distribution on tumor cell death after photodynamic therapy (PDT). BACKGROUND DATA: The photosensitizer accumulates in tumor tissue during PDT, and generates intracellular reactive oxygen species (ROS), resulting in tumor cell death. MATERIALS AND METHODS: This study was carried out to elucidate the effects of PDT in a KB oral cancer cell line using hematoporphyrin with irradiation at 635 nm and 5 mW/cm(2). After irradiation, the MTT reduction method, agarose gel electrophoresis, flow cytometry, and Diff-Quick staining were performed. The intracellular ROS level was measured by DCF-DA. Intracellular hematoporphyrin was monitored with a confocal microscope, and Western blot and caspase activity assays were performed. RESULTS: In our study, cell survival was reduced by about 50% after 3 h of hematoporphyrin incubation time. In DNA fragmentation, flow cytometry, and Diff-Quick assay, necrosis was identified within 12 h and apoptosis soon thereafter. Confocal microscopy revealed that hematoporphyrin was localized in the cell membrane, cytoplasm, and nucleus as time passed. The quantities of intracellular ROS correlated with the time of hematoporphyrin accumulation. Additionally, Western blot analysis of Bcl-2/Bax, the release of cytochrome C, and activity of caspase-3 and caspase-9 showed that apoptosis followed the mitochondria-dependent pathway. CONCLUSION: PDT with hematoporphyrin in the KB cell line showed morphological changes of cell necrosis and apoptosis, which were associated with the time of distribution and localization of hematoporphyrin. Also, the apoptosis evoked followed the mitochondria-dependent pathway.</P>
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치은 섬유아세포와 타액선 세포주에서 유지놀 처리에 따른 고사에 관한 연구
OkJoon Kim,HyangSuk Park,HongRan Choi 대한구강악안면병리학회 2004 대한구강악안면병리학회지 Vol.28 No.1
Eugenol (4-allyl-2-methoxyphenol) is a phenol derivative and generally used in dental treatment. A few investigator reported that eugen이-induced C)πoto잉city by apopto디c pathway, but it is not yet well understood In the present study, to investigate the eugenol-induced cytoto잉city by apoptosis, we have examined the apoptotic molecules and pathway in primary human gingival fibroblast (HGF) and human salivary gland cells (HSG). To identify apoptotic cell death, 3-(4,5-dimethylthiazol-2-yl)-2 ,5-diphenyl tetrazolium bromide (MTT) reduction assay with or without N-acetylcysteine (NAC), and the morphological study by propidium iodide (pI) staining were screened. And to investigate the apoptotic pathway, reverse transcriptase-polymerase chain reaction (RT-PCR) for apoptotic molecules and caspase aαivity assay were performed. Both M1T reduction assay and an addition of NAC showed that eugenol act as a pro-oxidant led to cell death. With the morphological study, both cells showed apoptotic change by nuclear fragmentation and/or chromatin condensations. With the apoptotic machinery study, the Bax and Bcl-2 mRNA expression were not detected in HGF. But, for HSG, the increased expression of Bax with decreased of Bcl-2 was observed. And the expression of Apaf-l was not detected or nα significantly increased in HGF and HSG, respectively. With measure of caspase activity, there was no change of caspase activities in HGF. But, for HSG, there was decrease of caspase 9 activity and increased caspase 3 activity. We suggest eugenol-treated HGF underwent apoptosis independent of Bcl family and caspase. However, for eugenol-πeated HSG, apoptosis occurred via Bcl famiIy and caspase pathway.
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Sun, Qiaochu,Kim, Hye-Eun,Cho, Hyejoung,Shi, Shuhan,Kim, Byungkuk,Kim, Okjoon Elsevier 2018 Journal of photochemistry and photobiology Biology Vol.186 No.-
<P><B>Abstract</B></P> <P>Oxidative stress, in which the amount of oxidants exceeds the capacity of antioxidant defense system, is a well-accepted pathogenesis of several human diseases. Light-emitting diode irradiation (LEDI) is an efficient strategy to counteract this condition. The biological effect of phototherapy, using visible light, has attracted recent attention especially in dermatological practice. However, little is known about the molecular mechanism of the anti-oxidant and anti-inflammatory effects of red light irradiation. We evaluated these effects of LEDI in HaCaT human keratinocyte cells under phorbol-12-myristate-13-acetate (PMA) induced reactive oxygen species (ROS). Microarray analysis revealed changes in 309 genes after LEDI. LEDI at 625 nm produced ROS scavenging and anti-inflammatory effects. One of the most important genes identified by microarray analysis was sphingosine kinase-1 (SPHK1), which is a key molecule in sphingolipid metabolism. SPHK1 knock-down drastically reduced ROS scavenging efficiency as well as expression levels of inflammation-related proteins in PMA-treated HaCaT cells. These results not only indicate the potential for the clinical application of 625-nm LEDI in treating skin disorders via ROS and/or inflammation, but also suggest SPHK1 as a potential therapeutic target in phototherapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> LEDI at 625 nm produced ROS scavenging and anti-inflammation. </LI> <LI> Sphingosine kinase-1 (SPHK1) was identified by microarray analysis in the experimental conditions. </LI> <LI> LEDI 625 nm has the potential for treating skin disorder via ROS and/or inflammation through SPHK1/NF-κB pathway. </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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