치주인대세포에서 Nicotine과 LPS에 의해 유도된 Human beta Defensin-2의 발현에 MAP kinase의 관여

서지정보

· 발행기관 : 대한구강악안면병리학회
· 수록지 정보 : 대한구강악안면병리학회지 / 35권 / 3호
· 저자명 : 이상임, 이화정, 배원정, 강순일, 이소윤, 이영만, 신경섭, 박재국, 류원국, 채종문, 김은철

목차

Ⅰ. 서론
Ⅱ. 재료 및 방법
1. 세포배양
2. Western 분석
3. EIA에 의한 PGE2 측정
4. 통계처리
Ⅲ. 결과
1. 니코틴과 LPS에 의한HBD-2와 COX-2 단백질의 발현
2. 니코틴과 LPS에 의한 MAPK 인산화에 대한 영향
3. 니코틴과 LPS에 의한 HBD-2, COX-2단백 유도 및PGE 생산에서 MAPK 억제자의 효과
Ⅳ. 고찰
Ⅴ. 결론
Ⅵ. 참고문헌

영어초록

Human β- defensin-2 (hBD-2) is an antimicrobial peptide which is produced by epithelial cells after stimulation with microorganisms or inflammatory mediators. However, little is known as to whether the LPS and nicotine induces the expression of hBD-2 in periodontal l igament (PDL) cells. T he p urpose o f this s tudy was t o investigate t he r oles o f MAPKs pathway o f nicotine a nd L PS-induced hBD-2 expression in PDL cells. The maximal expression of hBD-2 was observed in nicotine 5 mM and LPS 1 μg/ml treated PDL cells. Nicotine and LPS induced the phosphorylation of p38, c-Jun N-terminal kinase 1 and 2 (JNK1/2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2) MAPK. ERK1/2 inhibitor SB203580, p38 inhibitor PD98059, and JNK inhibitor SP600125, blocked the effects of nicotine and LPS on hBD-2 upregulation in PDL cells. These results collectively suggest that hBD-2 is up-regulated in nicotine and LPS-treated PDL cells through activation of p38, ERK and JNK MAPKs pathway. Our data regarding the up-regulation of hBD-2 may help us to understand the antimicrobial mechanism in periodontal disease

참고자료

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