국가연구개발성과
논문 (학술지)
Calcium regulates PMAP-23-induced apoptosis via mitochondrial disruption in Candida albicans
| 등록번호 | - | SCI 구분
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※구분 : SCI(SCIE포함), 비SCI |
비SCI |
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| 저자명 (주·공동저자) | 김수현 ; 이동건 ※ 과제 참여정보와 일치하는 연구자 상세정보로 정확하지 않을 수 있습니다. 동일저자 논문보기 |
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| 논문구분 | 국외기타논문집 | 학술지명 | - |
| ISSN | 0000-0000 | 학술지 출판일자 | - |
| 학술지 볼륨번호 | 0(0) | 논문페이지 | 1 ~ 10 |
| 학술지 임팩트팩터 | 0.0 | 기여율 | 100 % |
| 초록 | PMAP-23, derived from porcine myeloid cells, exerts antifungal activity against Candida albicans. Previous study reported that PMAP-23 damages plasma membrane at minimum inhibitory concentration (MIC). Although MIC showed membrane depolarization and pore formation activity, 1/4 and 1/8 MIC had no effect on plasma membrane. Interestingly, at 1/2 MIC, PMAP-23 depolarized membrane potential without membrane pore. Moreover, 1/2 MIC release K+ through the K+ channel unlike MIC. The present study suggests that the mechanisms of the two concentrations are different and we focused on antifungal mechanism at 1/2 MIC. C. albicans cells that exposure to PMAP-23 were induced phosphatidylserine exposure, caspase activation and chromatin condensation. The results demonstrate that PMAP-23 triggers apoptotic cell death. Additionally, we investigated the cause associated with apoptosis. PMAP-23 was able to increase of cytosolic and mitochondrial calcium level. Mitochondrial calcium uptake inhibitor, ruthenium red, recovered disrupted NAD+/NADH and reactive oxygen species (ROS) level caused by PMAP-23. It indicates PMAP-23-induced calcium homeostasis disruption caused excessive ROS generation. ROS scavenger N-acetylcysteine was used for demonstrating the effect of ROS on mitochondrial DNA and supported that mitochondrial DNA strand breaks along with generation of 8-hydroxy-2’-deoxyguanosine occurred. Consequently, ROS-induced mitochondrial DNA strand breaks lead to ultimate apoptotic cell death. In conclusion, PMAP-23 triggers mitochondrial calcium overload which leads to ROS overproduction followed by mitochondria-mediated apoptosis. | ||
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