Comet assay를 이용한 Ferric Sulfate의 유전자 독성에 대한 연구

박혜련,정태성,김신,강호승 大韓小兒齒科學會 2000 大韓小兒齒科學會誌 Vol.27 No.1

치수절단술은 유치의 치수치료 방법 중 사용빈도가 높은 시술 중 하나로 치수절단 술식에 사용되는 약제는 치수나 주위조직에 무해하여야 하며, 감염이나 내흡수 등의 부작용이 없어야 한다. 본 연구는 임상에서 유치의 지혈적 치수절단 술식의 약제로 사용되는 ferric sulfate의 유전자 독성을 평가할 목적으로 human gingival fibroblast에 ferric sulfate를 다양한 농도와 접촉시간을 설정한 후 comet assay를 이용하여 유전자 독성을 평가하여 보았다. 그 결과는 다음과 같다. 1. 농도에 따른 세포의 유전자 손상정도의 변화는 ferric sulfate의 농도에 비례하여 유전자 손상이 증가하는 양상을 나타내었다. 2. 농도에 따른 세포의 유전자 손상정도는 0.1,mM이상의 농도에서 대조군과 유의한 차이를 나타내었다.(p<0.05) 3. 시간경과에 따른 세포의 유전자 독성의 변화는 대조군과 유의한 차이를 보이지 않았다(P>0.05). Although ferric sulfate has been proposed as an alternative to formocresol in pulpotmy treatment in primary teeth, it has been given little concern regarding its cytotoxicity and mutagenicity. In the present study, we assessed the in vitro genotoxic effect of a ferric sulfate on human gingival fibroblast cell line (HGF-1), DNA damage was evaluated using comet assay (single cell alkaline gel electrophoresis) and obtained the results as follows: 1. A dose-response relationship was found between ferric sulfate concentrations (0 to 5mM)and DNA damages. 2. Above the concentration of 0.1mM, DNA damage was significantly increased than those of the control (p<0.05). 3. At the fixed concentration of 0.05mM, no significant difference was found between exposure time and DNA damage. These findings suggest that ferric sulfate as a pulpotomy agent can induce DNA damage in human gingival fibroblasts.

하악골에서 발생한 골아 세포종을 닮은 골육종의 치험 1례

이성근,정인교,박혜련 대한악안면성형재건외과학회 2000 Maxillofacial Plastic Reconstructive Surgery Vol.22 No.3

Typical osteoblastoma is generally considered to be a rare benign primary bone tumor that is seen primarily in children and young adults and curable by complete excision. However, the recurrence, aggressive behavior, or malignant transformation of this lesion was reported in some cases. It is reported that the malignant or aggressive osteoblatoma is really osteoblastoma-like osteosarcoma. Therefore, although this lesion is diagnosed as benign histologically. the operator must observe the postoperative course carefully. This article is to report a case of osteoblastoma-like osteosarcoma occurred in the mandible of 22 years old male patient with literature review.

Correlation between CD44 Expression and Biologic Behavior in Salivary Gland Tumors

Hae-Ryoun Park,Bong-Soo Park 대한구강악안면병리학회 1999 대한구강악안면병리학회지 Vol.23 No.1

Control of ASK1 Activity Via Protein-Protein Interaction

Hae Ryoun Park 대한구강악안면병리학회 2005 대한구강악안면병리학회지 Vol.29 No.5

ASKl(apoptosis signal-regulating kinase 1) is an important mediator of a poptotic s ignaling initi ated by a variety of death stimuli, including tumor necrosis factor ‘ Fas activat ion, oxidative st ress, and DNA damage. It was originally discovered as a mitogen -activated protein kinase kinase kinase(MAP3K) with proapoptotic activ ity Wben the A8Kl is stimulated, it activates both the MKK4/MKK7-JNK pathway and the M와(3/MKK6- p38 ki nase pathway‘ leading to stress responses or apoptosis. Owing to its critical role in promoting apoptosis. ASKl activity is highly control led in cells by multiple mechanisrns, includ ing phos ph이 ylation , oligomeri zation, and protein protein inte ractions. Phosphorylation of A8Kl at Thr-845 has been correlated with its acti vation . while phos phorylation at 8er-83 by Akt/protein kinase B attenuates A8Kl activity . It has also been demonst rated that in tramol ecular interaction, probably between the NH2• terminal and COOH-terminal domains of ASKl, may be required to maintain A8Kl in its inactive state, whereas oligomeri zation of its COOH- terminal domains is correlated with ASKl activation. The most commonly observed means of ASKl regulation, however, is thrO\땅h protein-protein in teractions. Numerous proteins have been shown to bind ASKl to exert theiJ‘ reg버atory function. For example. binding of TRAF2 0 1' Daxx promotes ASK1 funct ion, whereas the kinase and proapoptotic activities of A8Kl a re inhibited by many other associated proteins, including reduced t hi oredoxin, glutaredoxin, Cdc25A‘ Hsp 72, A8Kl - in teracting protein 1. and 14-3-3 proteins. A novel mechan ism of the anti-apoptotic action of Raf-l via phys ical interaction with ASKl wi ll be described. Furthermore, signifi cance of phosphorylati on s ite of 8er-1034 in the C-terminal regula tory domain of A8Klin the apoptotic activity wil l be discussed

K562세포의 apoptosis 유도에 미치는 저근백피의 효과

박혜련(Hae Ryoun Park),나문희(Mun Hee Na),윤용갑(Young Gab Yun),전병훈(Byung Hun Jeon),안원근(Won Gun An) 한의병리학회 2004 동의생리병리학회지 Vol.18 No.6

Delphinidin induces apoptosis and inhibits epithelial‐to‐mesenchymal transition via the ERK/p38 MAPK‐signaling pathway in human osteosarcoma cell lines

Kang, Hae‐,Mi,Park, Bong‐,Soo,Kang, Hyun‐,Kyung,Park, Hae‐,Ryoun,Yu, Su‐,Bin,Kim, In‐,Ryoung John Wiley and Sons Inc. 2018 Environmental toxicology Vol.33 No.6

<P><B>Abstract</B></P><P>Delphinidin is major anthocyanidin that is extracted from many pigmented fruits and vegetables. This substance has anti‐oxidant, anti‐inflammatory, anti‐angiogenic, and anti‐cancer properties. In addition, delphinidin strongly suppresses the migration and invasion of various cancer cells during tumorigenesis. Although delphinidin has anti‐cancer effects, little is known about its functional roles in osteosarcoma (OS). For these reasons, we have demonstrated the effects of delphinidin on OS cell lines. The effects of delphinidin on cell viability and growth of OS cells were assessed using the MTT assay and colony formation assays. Hoechst staining indicated that the delphinidin‐treated OS cells were undergoing apoptosis. Flow cytometry, confocal microscopy, and a western blot analysis also indicated evidence of apoptosis. Inhibition of cell migration and invasion was found to be associated with epithelial‐to‐mesenchymal transition (EMT), observed by using a wound healing assay, an invasion assay, and a western blot analysis. Furthermore, delphinidin treatment resulted in a profound reduction of phosphorylated forms of ERK and p38. These findings demonstrate that delphinidin treatment suppressed EMT through the mitogen‐activated protein kinase (MAPK) signaling pathway in OS cell lines. Taken together, our results suggest that delphinidin strongly inhibits cell proliferation and induces apoptosis. Delphinidin treatment also suppresses cell migration and prevents EMT via the MAPK‐signaling pathway in OS cell lines. For these reasons, delphinidin has anti‐cancer effects and can suppress metastasis in OS cell lines, and it might be worth using as an OS therapeutic agent.</P>

구강 편평세포 암종에서의 CD44 발현

박상준(Sang Jun Park),박혜련(Hae Ryoun Park),김규천(Gyoo Cheon Kim),박봉수(Bong Soo Park),김태규(Tae Kyu Kim) 대한구강악안면외과학회 2000 대한구강악안면외과학회지 Vol.26 No.2

The cell surface glycoprotein CD44 is a kind of adhesion molecule, which binds hyaluronic acid, type I collagen and fibronectin. Although there have been numerous reports on the expression and the function of CD44 in lymphocytes and macrophages, very little is known about its distribution and definite role in epithelial tissue, especially in oral epithelial one. The present study was performed to investigate the distribution and expression of the CD44 in human gingiva and squamous cell carcinoma(SCC) arising in human gingiva. And the authors compared CD44 expression with histopathologic grade of SCC. The results were as follows: 1. The CD44 was strongly expressed in granular, spinous and basal layers of normal marginal and attached gingiva, in spinous and basal layers of normal sulcular gingiva, and in all epithelial layers of normal junctional gingiva. 2. In SCC of gingiva, the CD44 was expressed in all but one case. In most of the cases the CD44 was expressed at cell membrane and the degree of expression was relatively strong. 3. In low-grade SCC of gingiva, the CD44 was strongly expressed, especially at the basal and spinous layers of abundantly keratinized cancer nests. In high-grade SCC of gingiva, the CD44 expression tended to be weak but was strong at cells showing individual keratinization. This study suggest that the CD44 expression of normal and cancerous gingival epithelium is associated with the degree of proliferation and differentiation of epithelial cells.

MAPK3 at the Autism-Linked Human 16p11.2 Locus Influences Precise Synaptic Target Selection at Drosophila Larval Neuromuscular Junctions

Park, Sang Mee,Park, Hae Ryoun,Lee, Ji Hye Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2

Proper synaptic function in neural circuits requires precise pairings between correct pre- and post-synaptic partners. Errors in this process may underlie development of neuropsychiatric disorders, such as autism spectrum disorder (ASD). Development of ASD can be influenced by genetic factors, including copy number variations (CNVs). In this study, we focused on a CNV occurring at the 16p11.2 locus in the human genome and investigated potential defects in synaptic connectivity caused by reduced activities of genes located in this region at Drosophila larval neuromuscular junctions, a well-established model synapse with stereotypic synaptic structures. A mutation of rolled, a Drosophila homolog of human mitogen-activated protein kinase 3 (MAPK3) at the 16p11.2 locus, caused ectopic innervation of axonal branches and their abnormal defasciculation. The specificity of these phenotypes was confirmed by expression of wild-type rolled in the mutant background. Albeit to a lesser extent, we also observed ectopic innervation patterns in mutants defective in Cdk2, Gq, and Gp93, all of which were expected to interact with Rolled MAPK3. A further genetic analysis in double heterozygous combinations revealed a synergistic interaction between rolled and Gp93. In addition, results from RT-qPCR analyses indicated consistently reduced rolled mRNA levels in Cdk2, Gq, and Gp93 mutants. Taken together, these data suggest a central role of MAPK3 in regulating the precise targeting of presynaptic axons to proper postsynaptic targets, a critical step that may be altered significantly in ASD.

모반양 기저세포암종 증후군

박혜련,한영임,설미영,이선경 대한병리학회 1995 Journal of Pathology and Translational Medicine Vol.29 No.2

Acetylshikonin suppresses invasion of <i>Porphyromonas gingivalis</i> -infected YD10B oral cancer cells by modulating the interleukin-8/matrix metalloproteinase axis

Cho, Bong-Hae,Jung, Yun-Hoa,Kim, Da Jeong,Woo, Bok Hee,Jung, Ji Eun,Lee, Ji Hye,Choi, Young Whan,Park, Hae Ryoun SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.2

<P>The development of pharmaceutical agents possessing anti-invasive and anti-metastatic abilities, as well as apoptotic activity, is important in decreasing the incidence and recurrence of oral cancer. Cancer cells are known to acquire invasiveness not only through epigenetic changes, but also from inflammatory stimuli within the tumor microenvironment. Accordingly, the identification of agents that can suppress the inflammation-promoted invasiveness of cancer cells may be important in treating cancer and improving the prognosis of patients with cancer. Acetylshikonin, a flavonoid with anti-inflammatory activity, inhibits proliferation and induces apoptosis of oral cancer cells. In the present study, the anti-invasive effect of acetylshikonin on YD10B oral cancer cells infected with <I>Porphyromonas gingivalis</I>, a major pathogen of chronic periodontitis, and the mechanisms involved were investigated. Firstly, we examined whether <I>P. gingivalis</I> infection increased the invasiveness of YD10B cells. Results suggested that YD10B oral cancer cells become more aggressive when they are infected with <I>P. gingivalis</I>. Secondly, acetylshikonin significantly inhibited the invasion of <I>P. gingivalis</I>-infected YD10B cells by suppressing IL-8 release and IL-8-dependent MMP release. These data suggest that acetylshikonin may be a useful preventive and therapeutic candidate for oral cancer that is chronically infected with periodontal pathogens.</P>