간행물
대한구강악안면병리학회지 KCI 등재 The Korean Journal of Oral and Maxillofacial Pathology
- 발행기관 대한구강악안면병리학회
- 자료유형 학술지
- 간기 격월간
- ISSN 1225-1577 (Print)2384-0900 (Online)
- 수록기간 1977 ~ 2024
- 주제분류 의약학 > 치의학 의약학 분류의 다른 간행물
- 십진분류KDC 515DDC 610
권호리스트/논문검색
제29권 제5호 (2005년 10월) 33건
21.
2005.10
구독 인증기관·개인회원 무료
구강암의 발생원인 중 하나인 인간유두종바이 러스(HPV)로 불멸화시 킨 구깅 각화세 포(1 HOK) 외 정상 인긴 구강각화세 포 (NHOK) 의 표지자를 비 교 연구하는 것은 정상과 그 전암냉소의 생화학적 및 세 포회 학적 띤호l을 평가히는 적젤힌 모탤이지띤 떤 구된바 많지 않았다 본 연구는 구강 각화 세 포의 형 질전환을 조절히는 분자적 상태를 연구하기 위 해 익 6000711 의 유전자가 pri nt된 cONA mì croarray를 이용하여 인간 정상 구강각화세 포(NHOK) 와 HPV16으로 불띨회한 각화세 포(J HO K) 간에 유전지 발현을 비교하였다， NHOK외 IHOK세포는 96%의 유전자가 유사한 발현을 보였으며 2배이 상의 발현을 보이 는 경우-는 NHOK가 IHOK에 비해 85개 유전지가‘ IHOK가 쩌OK에 비해 1477H 의 유전자 발현이 u p-regul at i on되 어 총 4%미 만이 발현차이를 보 였고 반복된 hybridì zation 으로부터 얻은 선택된 spot의 Pearson 싱관계수는 074 에서 091로 냐티 났다 NHOK외 IHOK간의 유전자 발현을 기능별로 분석한 결과 몇 가지 주요 발현 유전자 그룹을 확인하였는데 세포부착 및 인식 세포주기 초칠인지 세 포자떨사， 전사인지- 성장인자 및 수용기 ， 세포골격 및 세 포외기질 단백 . 신호진달 조절자 및 기 타 그룹으로 분류할 수 있었다 IHOK에서 는 세 포인식 인자 중 endothelin 1, collagen IV, fibronectin , SPR1 이 발현증가 되었고 CK7, POG1"2, F'G1"1"R2가 세 포골격 및 성장인지중에서 upregulation 되었지만 신호전달 인지중 발현증가된 것은 없었고 동일힌 유전자를 나타내 는 cJ ustered gene map을 그릴 수 있었다 따라서 이러힌 Illicroan‘ay를 이 용한 분자학적 표지자 얀구가 구강 임 빌임과정 에서 유전지발현 을 확인히는데 큰 도웅을 줄 수 있을 뿐 아니라 유전자 조절에 의힌 진단 에 후. 치 료의 정획성을 개선시 킬 수 있으리리 여겨진다
22.
2005.10
구독 인증기관·개인회원 무료
Hwa Jeong Lee, Sun Kyung Lee, Han Young Guo, Suk Ho Kim, Sung Hyun Kim, Dal Ho Won, Jong Dae Park, Eun Cheol Kim
Interlellkin • 8(IL-8) is an important cytokine involved in tllmor growth and angiogenesis in a variety of malig nancies. bllt the regll lation of IL-8 in 01 외 cancer cells are llnderstood . We invesLigated whether mi togen-activated protein kinases pathway is involved in iron chelator-mediated lL-8 produdion in inunortalized and malignant oral keratinocytes. In this study we examined the role of p38 and extracellular signal- reglllated kinase• 1/2 in the expression of [L-8 by DFO. Incllbation of IHOK and HN12 cel ls with DF'O increased the expression of 11-8 mRNA. as well as the release of IL-8 protein. The signal transdllction study revealed that both p38 and ERK1/2 were significantly activated in response to DFO. Accord ingly. the selective inhibitors for both kinases‘ eit her a lone or combination. abolished DFO- induced lL-8 secretion. indicating an importance of MAP kinase pathway. Interestingly. however‘ inhibition of the p38 and ERK pathway more attenuated IL-8 secretion in IHOK than in HN12 cells. DFO induced NF-kB activation , suggesting a NF-kB- dependent mechanism in DFO- induced IL-8 production. In addition, p38 and ERK inhi bition resulted in the accelerated degradation of lL-8 mRNA, suggesting that in IHOK and HN12 cells, p38 and ERK cunLr iullLe Lo DFO imluced IL-8 secretion by IHOK and HN12 cells via a posttranscriptional mechanism that involves stabilization 01' the IL-8 transcript. Finally. we investigatecl llsing specific inhibitors : 8NP and G8NO for NO c1onor. PDTC for potent inhibitor of NF-kB. Cycloheximide for inhibition of de novo protein synthesis. We observecl 8NP ancl PD1'C clepenclent IL-8 gene incluction in IHOK cell s. but not in HN12 cells used specific inhibitors‘ Collectively. these results demonstrate that‘ targeting MAP kinase ancl NF-kB pathway may be a potentiaI approacb to controlling the angiogenes is ancl growth 이 human oral cancers
23.
2005.10
구독 인증기관·개인회원 무료
1'0 determine Lhe ll1echanism of cell c1eath incluced by iron chelators. we explored the pathways of the three structurally relatecl ll1 itogen-activatecl protein(MAP) kinase subfami li esduring iron cbelator- inclucecl apoptosis ancl differentiation of oral precancerous ancl cancel‘ cells. The iron chelator c1 eferoxamine(DFO) exertecl potent timeancl c1ose-c1epenclent inhi bitory effects on the growth of IHOK and HN4 cells The major mechanism of growth inhibition following DFO treatment was fOllncl to be apoptosis incluction. as assessecl by annexin V-FITC staining. cell cycle analysis‘ DNA lacldering, a ncl Hoechst staining. We report that DF'O s trongly activates the p38 MAP kinase and extracell ular signal- regu lated kinase(ERK). but c10es not activate the c-Jun N-terminal kin ase/ stl않s-activaLecl protein kinase(JNK/8APK) . Of the three MAP kinase blockers usecl‘ the selective p38 MAP kinase inhibitor 8ß203580 ancl ERK inhibitor PD98059 protected oral premaIignant ancl malignant cells againsL iron chelator- nclllced cell death. which incl icates that the p38 MAP kinase serves as a major mecliator 01' apoptos is induced by this iron chelator DFO also evoked the release of cytochrome c from mitochondria, and incluced the activation of caspase-3 ancl caspase-8 in oral cancer cells, which suggests that apoptosis occurs via the mi tochoncl ri on - mecl iaLed pathway. DFO enhanced the expression of Bax in IHOK ancl HN4 cells. consistent witll thei r p53 status Moreover. DFO downregulatecl the expression 01' Bcl-2 in oral cancer cells. which suggests that DFO- incluced apoptos is 01' oraJ cancer and precancerous cells may be mediatecl by an increase in the ratio of pro-apoptotic to anti-apoptotic proteins. ln terestingJy, trcatmcnt 01' IHOK ancl HN4 cel ls with 8B203580 abolishecl cytochrome c release‘ as wel l as the activation of caspase-3 and caspase-8. DFO suppressecl the expression of epithelial di ffe rentiation markers, such as involucrin, t ransglutaminase II. CK6. and CK19. ancl this suppression was blockecl by p38 ancl ERK MAP kinase ll1hlbltors The oral premalignant(IHOK) ancl malignant cell s(I-lN4) showed differential responses to DFO with respect to the expression of cel l cycle regulatory proteins. cell growth. ancl apoptosis. Coll ectively. the current study reveals that p38 MAP kinase plays an ill1 portant role in iron chela tor-mecliatecl cel l cleath and in the suppression of differentiation of oral premalignantandmalignanLcell s.by activating a c10wnstream apoptotic cascade that executes the ceIl c1eath pathway
24.
2005.10
구독 인증기관·개인회원 무료
Mecke!'s car t ilage is one of the ea rliest structu re to appear in a mandible derived from the lï rst branchi a l a rch and serves as the primorclium I"or the formation 01‘ mandible‘ mall eus. incus. and sphenomandibular li gament However. its direct role a nd the mechanism in mandibular clevelopment a re not well elucidated. 1'0 address t his Issue‘ we observed morphol ogical and histological changes and gene expression patterns in the Mecke!'s cart ilage 01" a cleveloping mouse. I"rom E13.5 to E18.5 embryos. using skeletal preparation samples a ncl routinely prepa red s lide secti ons for light mi croscopic observation in various sectional planes. The following methods were per |‘ ormecl : H&E staining I"or general hi st이 og i cal observation ‘ Von Kossafor detection of minerali zation. TRAP activ ity staining for locali zaLion 01’ osteoclastic cell s. immunohistochemistry for !Iα@-1 a ncl -9 forevaluati on of enzy matic activity 01" osteoclasLic cell s. a ncl in situ hybricli zation for detection of collagen type 1. Il. ancl X mRNA ex presslon‘ respecLively. AL E1 3.5 Mec kel's cartilage appeared as a V-shaped rod fused a t the micl line and thin minera li zed ma ndibular buccal plaLe was I"ormed lateral to. and at some clistance from. Meckel’s carti lage in an intramembranous ossi lïcation mocle. WiLh the progression of tooth development. t he Meckel’s in carti lage adjacent incisors revealecl hyperLrophi c chonclrocyte di ff"er entiation with minerali zation of the chondroid matrix. The Meckel’s car Li lage was replacecl with bone by o~ L eoc l asLs . showing strong immunoreact ivity for MMP- l ancl -9 from E16 5 Wi Lh ti me‘ Lhis bony replacement of Meckel's cartilage in an endochondral ossification mode was ex Lenclecl up Lo the mid-porLion of Lhe molar sockets til l EI8.5. The bony replacement of minera li zed hypertrophic chondrocyte zone expressing X collagen mHNA conLri buted to the formation of thick mandibular lingual plate . 1'hese f"i ndings suggesL LhaL mandibular formalion and development is closely relatecl with not only Mecke!'s carLi lage. buL also wiLh Lhc developing LooLh. and thaL C'erLai n in f"l uence from the developing tooth may play a role in detcrmin in g Lhe faLc of Meckel’s ca rLi lage cluring ma ndi bular development.
25.
2005.10
구독 인증기관·개인회원 무료
Cellular imrnortali zation is thought to be an ear ly event during tumorigenesis. Telomerase reacLi vaLion by ecLopic hTERT expression is widely used for cellular imrnortali zation. This study was a imed Lo a na lyze establi sh immortalized human ora l epithelial cells(IOEC) and to reconstruct oral precancerous lesion by Lhree dimens iona l cultures. Telomerase activity was analyzed by Telomerase assays and Telomere longLh W:lS dcLccLcd by Termina l restri ction I"ragment analysis. bTERT gene was assayecl by tbe RT-PCR. p16lNK4 a‘ pHb. CDK2. P21CIP1. p27 and p53 were examined by western blotting. Three dimensiona l cu1ture using air - liquicl inLe rl"ace was pe rl"ormed. As results. IOEC was establi shed by ectopic ex pression of catalytic subunit• of telomerase‘ h1'EH1'. which is con tinuously maintained for more tban 120 population doublings(PDs) . IOEC showecl the expression 01" h1'ER1' and h1'H mHNA‘ elongated telomere length and higher telomerase activity. These cel ls showed no ex pression of p16lNK4a with retention 01" pRb and CDK2. Expression of p21CIP1. p27 a nd p53 may have no relation to immorta li ze oraJ epithelial cell s. Three dimensional culture of IOEC showed dysplastic strat ilïed epithelia l cell s. These results may serve as a useful moclel system for the study of oral carcinogenesis.
26.
2005.10
구독 인증기관·개인회원 무료
Gene reg비 at i o n during the human craniofacial development is not well understood In effort to understand n ewly identifï ed genes that may play role(s) in the human craniofacial development, non-redundan t genes were isolated from the s ubtracted cDNA libra ry of human embryonal craniofacial tissues and examined their possible structu ral rolc in parallcl with thosc gcncs from isolatecl human c h o nclroc)πes cDNA library. Fifty genes were init ia ll y chosen from 398 clones iso latecl were used for selective dominant expression in both chondrocytes and the craniofacial sections of 10 weeks old human embryo by in situ hybridization method. Based upon the high levels 。f expression, we have identifi ecl seven unknown genes; ch89, ch96. ch129. ch 153. ch 276 ch285. and ch334 . In 。rder to unde rs tancl the possi ble role of these genes‘ the structural simulation of the expressed proteins were constructecl by Sybyl 6.6 program. Ch 276 gene was same with a clone, c14 0 1' f173. registered in GenBank(NM_022489) a nd is composed 0 1' 323 amino acids having a reverse s ignaling domain from the extra- cellular matrix(C-terminal) to cell membrane(N-terminal) and 12 turns of helical structure. Gene protein also r etains a famil iar fïbronectin binding domain(RGD). three s ites 0 1' Ca ion binding motifs. cAMP- and cGMP-dep endent protein kinase phos phorylation site, two regions of protein kinase C phosphorylation s ites. glyco- saminoglycan attachment s ite ancl N-glycosylation site. transmembrane and Al kaline Phosphatase active s ite domains This newly iclentifï ed human protein from human choncl rocytes cDNA library appearecl to be related to a known calcification s ignaling protein. was named as Ca lsin(Ch276) . Ch153 appeared to be related a family of anti-microbial peptide acting as an inflammation mediator and Ch334 clone as a zinc finger protein whose expression in creases in human adult ti ssue‘ These results suggest that these novel genes ident i!ï ed from human chondrocytes rnay provide a new path 0 1' embryonic cartilage development and human craniofacial development.
27.
2005.10
구독 인증기관·개인회원 무료
gp130-Mediated signaling is involved in both chondrogenesis and osteogenesis. but its direct role in the mecha nism of embryonic Meckel’s cartilage and associated mandibular development has not yet been elucidated . In this s tudy. we examined the influence of gp130 ablation on the morphogenesis of Meckel’s cartilage and subsequent d evelopment of mandible by evaluating the morphological and histological changes as well as the gene expression patterns in developing embryonic gp130 deficient Ullce The abla tion of the gp130 gene showecl 110 change in region- specific collagen mRNA expression except for a s light delay in its expression but caused shortened embry 。nic Mecke]'s cartilage, delayed hypertrophic chondrocyte maturation and subseqllent bony replacement with characteristic bending of the intramandibular Meckel's cartilage. The bending 0 1' Meckel's cartilage leads to a narrow mandibular arch at the rostral area with poor cortical plate formation. These fir띠 ings indi cate that gp130 is im p ortant for the normal morphogen않is 01' Meckel's cartiJage and sllbsequent mandib띠a‘ c1evelopmen
28.
2005.10
구독 인증기관·개인회원 무료
본 연구는 연역조직 회학 방법 및 in situ hybridization 법을 이용하여 골 치유 과정중의 골성 장 반응 빛 골 기질 단백질 형성이| 관여하는 여러 성장인자 및 골기질 관련물질에 대한 변화를 알아보고자 하였으며 특히 임 플란트 배식 후 티티늄 표연과 인접한 주변 골에서 나타나는 다양한 골기질 단백질의 형성과 골 성장과 관련한 성장인지들의 변화를 관칠하고자 히였디 직경 3 -5mm의 thread - ed implan t를 백서 장골에 매 식한 후 시 간적 변화에 따른 골기질 관련 물질 및 관련 mRNA의 분포변호}를 관찰히였다 디1 상은 콜리 겐 . osteonectin(ON). osteopontin(OPN). osteocalcin (OC) 동의 분포의 변호}를 연역조직화학적 방법으로 보고 이와 힘께 골기질 형 성관련 성장인자인 VEGF와 ON 의 l알헌을 in situ hybricli za tion 법을 이용해서 관찰하였다 3일째 소견에서 는 골 내부에 형성된 나사 산과 잉프란트의 강제적인 접 촉으로 인해서 높은 접촉률을 나티내고 있었으나‘ 부위에 따라서는 혈벙으로민 둘러씨인 부분도 관칠되었 다 7일째 소견에서 는 이 같은 인위적인 접촉부위에서 골 흡수가 일어니연서 골접촉이 크게 감소하였다 7 일과 14일에서 골의 형성은 이주 낮은 정도로 나타났으마. 14 일째에 는 골 집촉의 증기기 다소 나타나지만 골 밀도는 골의 게조로 인해 김소하는 소견을 나타내 었 다 연역조직화학적 염색에서 대조균은 콜라겐이 결합조직 에 서 항상 강한 양성 반응을 보였다 반면 실험군에서는 신생 골에서 일부에 서만 약한 양성 반응을 보였다 OC은 신생골에서는 거의 관찰되지 않았으며 기존 골의 손상부위에 부분적으로 양성 만응을 보였다 OPN은 결함조직 에서 강한 양성 반응을 보였으며 신생 골의 골양 조직과 골소공 주변에서 양성반응을 나타내었다 ON은 기존골의 일 부와 신생골에서 관찰 되었다 특히 골모세포와 골세포에서 양성반응을 나타내 었다 대조군과 실험군들 간의 연역조직화학적 염색에서 의 뚜렷한 차이는 보이지 않았다 OC은 대조군에서와 마찬가지로 신생골에서는 거의 관찰되지 않았으며. 인접 골 주변부에서 부분적 으로 양성 반응을 보였다 OPN은 대 조군과 실험군 동일하게 결합조직 에서 강한 양성 반응을 보였으며 신생골의 골양 조직과 골소공 주변에서 발현되는 것도 유시하였다 ON의 말현 OJ상도 대조군의 경우와 통일하였으며 골모세포나 골세포 에서 양성 반응을 나티 내 띤 서 골질에 대해서 는 신생골이니 골 게 조 후의 골보다 석회화가 어느 정도 진행된 골 개조 이전의 골에서 뚜렷한 양성을 보였다 ON 의 발현잉상에서 연띄조직화학 염색소견과 달러 골기질 단백질의 형성과정에서 나타나는 세포내 mRNA의 발현은 임플란트에 보다 근 접힌 세포에서 발현이 증가히는 깃이 관찰되었다 이상의 결과에서 얻은 겔론은 다음과 같다 i 소형 임플린트의 떼식 시 나타나는 조직 띤응은 정싱크기 의 임 풀란트에서외 동일힌 소견을 나타내았다 2 골재생은 3일 째부터 관칠되었으며 14 일이후 골재소가 나티니 21 일까지 지속되었다 3 임플란트 주맨에서 나타냐는 골재생관련 성장인자외 골기질 단백질은 골결손으로 인한 재생 시와 동일한 소 낀을 니 타내 었다 4 띤약조직화흐l 염색소견과 달리 골기질 단백질의 형성과정에서 나타나는 세 포내 mR NA의 발현은 임플란트에 보디근접한 세포에서 발힌이 증가히는 것이 관찰되었으며 이는 임풀란트 제 료의 표면이 골형성 유도능을 가진 것이기 보다는 골형성 유도 능을 가진 세 포외 인지들이 티타늄 표띤 애 수동적으로 홉착됨으로 잔존 기간이 증가하고 이동성이 감소함으로서 나타나는 현상으로 보인다 5. 티타늄 인 플렌트의 표띤은 특띨힌 처리 없이 도 곧형성 유도른 증가시 키는 것으로 보인다
29.
2005.10
구독 인증기관·개인회원 무료
본 연구는 SPARC(osteo n ect in) 이 석회화 물질의 형성에 밀접한 연관을 가진다는 짐 애 착안하여 골조직 재생 괴정 중의 기질-세포 상호자용에 있어 SPARC의 역할 석회화 조직 형성과 연관된 SPARC의 발현조절과 기능을 규명하고자 시행되었다 l꾀서 태자 두개관 배양세포로부터 SPARC cDNA를 합성하였으며 이를 이용하여 백서 SPARC 단백질을 합성하였다 SP때C 단맥 질을 이용해 백서 조골 세 포의 증식 에 미치는 영호노을 관찰하였다 동시 에 백서 장골에 인위적인 골결손을 형성하고 형성과정에서의 골기질 관련인자의 분포를 관찰하고 SPARC 의 분포를 in situ hyb ridiz a tion법을 이용하여 관찰하였다 백서에서 분리 합성된 cDNA 조각은 1231bp 크기 였으며 40kD 크기의 단백질을 발현하였다 백서 태자 두개관 세 포의 증식에서 SPARC과 콜라겐 으로 처리된 표띤은 콜리겐 단독으로 표면처 리된 t111 양표연보다 증가힌 세포증식과 단백질 합성 콜라겐 합성을 나티내 었다 백서 -?I-골이1 형성힌 골조직 지| 생괴정에서 SPARC을 투여힌 백서 ;<J-골의 경우 결손부 전체에 걸쳐 증가한 SPARC의 합성을 보였디 SPARC이 투여된 군에서는 질손부의 중심 에서부터 SPARC과 콜라겐의 합성이 증기한 양상을 나타내었으며 대조군과 뚜렷한 차이를 나타내었다 in siLu h yb ricli za Li o n 깨 을 이용한 관칠 에서 골결손부 중잉에 있는 세 포에서의 SPARC 발현이 증가하였으며 그 싱패는 1 4 일 까지 대 조군에 비해 높게 니티났디 이싱의 연구 에서 얻은 결론은 디음과 같다 SPARC은 콜라겐과 결합하여 백서태자 두개관세 포의 배양에서 세 포증식 및 단백질 한성 ‘ 콜라겐 합성 의 뚜렷한 증가를 나타내었으며 . 이 같은 OJ상은 SPARC 단독으로 표연 처리하였을 때 는 관찰되지 않았다. SPARC의 골절손부 투여는 골조직 의 재생을 촉진허며 초기 세 포외 기질의 합성을 증가시켰으며 특히 SP뻐C의 형성이 초기애 증가하는 앙싱 융 나타내었다 이상 의 결과로 볼 떼 SPARC의 투여는 골조직 손상회복 시 초기 골기질 형성과 석회화에 영향을 미치며 SPARC 자치1 의 형성 증가에도 영향 을 미치는것으로보인다
30.
2005.10
구독 인증기관·개인회원 무료
Hereditary dentin defects consists of dentin dysplasia(DD) and denti nogenesis imperfecta(Dr) ‘ The Dl associated with osteogenesis imperfecta has been classified as DI type 1. whereas isolated inherited defects have been categori zed as DI types II and III , However‘ whether DI type III should be considered a distinct phenotype 01' a variation of DI type 1I is debatable , Recent genetic findings have focused attention on the role of the dentin sialo phosphoprotein(DSPP) gene in the etiology of inherited defects of tooth dentin, We have identified novel mlltation( c,727G - > A, p,D243N) at the 243th codon of exon 4 of the DSPP gene in a Korean patient with DI type III The radiographic and histologic features of the patient revealed the classic phenotype of shell teeth These findings sllggest that DI type II and III are not separate diseases bllt rather the phenotypic variation 01' a s ingle disease
31.
2005.10
구독 인증기관·개인회원 무료
rt is well known that glycosaminoglycans are 01' fllndamental importance to the processes 01' morphogenesis and cytodifferentiati on dllring the teeth development , With HlD-TCH-SP(High - iron diamine-thiocarbohydrazide-silvel protcinntc) , s lllfatcd glycosaminoglycans such as chondroitin sulfate and heparan slllfate have been localized a t the III trastrllctural level i n a wide variety of tlssues The pmpose of this stlldy were to examine slllfated glycosaminoglycan at llltrastrllctllral level fo 1' the phase of morphogenesis and cytodifferentiation of hllma n fetal tooth germs, and to detect the protein expression of slllfated glycosaminoglycan by immunoslot blot Human tooth gerll1s fl'Oll1 the a lveolar bone of twenty still born fetuses we1'e fixed in a mixtllre of 2% gllltaraldehyde/1% forma ldehyde, The 미 t 1'athin sections were stained witb HID-TCH-SP and were treated with 0, 05% solution of t esticular hyaluronidase to identify the histochemical properties 01' tbe HID-TCH-SP stain deposits , For semi quantitative protein assay , immllnoslot blot was done Sulfated glycocongugated deposits were localized in DEJ, peri tubular dentin , and mantle dentin matrix‘ enamel prism sheath , interrod area , and enamel matnx Heparan sll l띠 te deposits i n DEJ resisted to testicular hyalllronidase treatment prior to HID-TCH-SP staining, Immunoslot blot s howed that• chondroitin sulfate was detected higher in enamel and dentin extract, while heparan sulfate was relatively expressed in enamel and dentin extract, but rarely expressed in enamel or dentin extract It suggest ecl that chonclroi tin and hepa ran slllfate woulcl play an important role in the formation of DEJ, while chondroitin sulfate would in the clevelopll1ent of enamel prism sheath, enamel matrix, and mantle 01' peritublllar clentin of human fetal tooth germs,
32.
2005.10
구독 인증기관·개인회원 무료
Kyung San Min, Young Hee Hwang, Hyun Jin Ju, Hoon Sang Chang, Kyung Hwa Kang, Sung Hee pi, Sun Kyung Lee, Eun Cheol Kim
This study was to taken to demonstrate the effects of exogenous nitric oxide(NO) on hu rnan pu lp cell s ‘ In volvement of cyclic 3’, 5' -monophosphate(cGMP) in p버 paJ protection induced by herne oxygenase-l (J-lO-l) against NO-induced cytotoxicity , By use of Western blotting and cell viabi lity assay, we have examined the cytotoxicity and J-lO-l induction in pulp cells that were treated with NO donor ‘ S-nitroso-N-acetyl-D, L-penici 1 lamine(SNAP) , We have assessed wheathel' HQ--l contributes the cytoprotective effect against the cytotoxicity caused by NO, and inves tigated the l'elationship between HO-l and cGMP in the s ignaling pathway, SNAP decreased cell via bility but in creased HO-l expl'ession in a concentl'ation- and time一dependent manner in hurnan pu lp cells NO-induced cyto toxicity was inhibited in the presence of the hemin(inducer of HO-l) , whel'eas was en hanced in the pl'esence zinc protoporphyrin IX(ZnPP IX, HO-l inhibitor), thus Lhe NO-induced cytoLoxicity was cOl'related with HO- l expression. R‘ etreatment with a rnemhrane-permeable cGMP analog, 8-bromo-cGMP, restored cell death and enhanced the HO-l protein expression induced by SNAP, ln contrast‘ inhibition of guanylate cyclase by lI-l -[1,2,4] ox adiazole[ 4,3 口]quinoxalin-l-one(ODQ) pretreated pulp cells to 1 mM SNAP resulting in marked cytotoxicity , These findings , demonstrating a link between J-lO-l, regulated thl'ough the cGMP system and NO-induced cytotox.icity in huma띠 p버 p ceJls , suggesti ng a protective 1'ole of HO-l in pulp infl ammatory disease
33.
2005.10
구독 인증기관·개인회원 무료
Jae Hyuck Yang, Youn Young Jang, Kwon Jung, Mi Kyeong Ko, Mi Sun Jang, Eun Byul Kook, Chae Kwang Lim, Won Bong Lim, Jin Soo Park, Ok Joon Kim, Hong Ran Choi
The purpose 01' pl'esent study was to examine the molecular events in apoptosis by CoCl2, mimicking hypoxic cond ition and recovering effects by LED ir l'adiation on Human SH-SY5Y neuroblastoma cells The SOUl'ce 0 1' light for ir l'adiation was a continuous-wave LED emitting at a wavelenl양h of 590 nm, and manufactured that ene rgy density was 5 mW!cm2 on sample surface, After ir l'adiation, cell viabi lity was measured with BrdU , cell morphol ogy was examined with Diff- Quik staining, cell signaling was monitored with various apoptosis-related molecules using RNase Pl'otection Assay(RPA) , W11en treated with CoC12, apoptotic induction was found in the SH-SY5Y cells in a concentration-dependent and time-dependent manner , Diff-Quik s taining was revealed that DNA fragmentation re presented apoptosis was examined in CoC12-tl'eated group, Moreover, RPA assay of SH-SY5Y cclls lIs ing val'iolls apoptosis-related molecllles showed that the apoptotic cell population was mcreased J-loweve. there was sorne signifïcant change in LED irradiatied cells aftel' treatement of CoC12 The main mechanism for Lhese a poptosis appearecl to be mito c hondriεt - m ecliated pathway, such as cytochrome- c‘ caspase-9, caspase-3, pro-apototic protein ßax, anti-apototic protein Bcl-2, and death receptor• mediated pathway, such as Fas, cas pase- 8, a ncl TNFRl These results demonstrate that CoCI2 induce apoptosis in SH-SY5Y via different dual apop tosis pathway through death receptor pathway as well as mitochondria- dependent pathway and LED irradiation can recl llces the CoCl2-induced apoptosis by blocking their internal signaling pathway
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