메뉴 건너뛰기
.. 내서재 .. 알림
소속 기관/학교 인증
인증하면 논문, 학술자료 등을  무료로 열람할 수 있어요.
한국대학교, 누리자동차, 시립도서관 등 나의 기관을 확인해보세요
(국내 대학 90% 이상 구독 중)
로그인 회원가입 고객센터 ENG
주제분류

추천
검색

논문 기본 정보

자료유형
학술저널
저자정보
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제52권
발행연도
2020.1
수록면
1 - 12 (12page)

이용수

표지
📌
연구주제
📖
연구배경
🔬
연구방법
🏆
연구결과
AI에게 요청하기
추천
검색

초록· 키워드

오류제보하기
Spinal cord injury after surgical repair of the thoracic or thoracoabdominal aorta is a devastating complication that is associated with pathological changes, including inflammation, edema, and nerve cell damage. Recently, microRNA (miRNA)-modulated control of spinal cord injury has been actively investigated. This study aims to clarify the regulatory effect of miR-214-mediated inhibition of Kcnk2 following spinal cord ischemia-reperfusion injury (SCII) and the possible underlying mechanisms. SCII was induced in rats by occluding the aortic arch followed by reperfusion. Gain-of-function and loss-of-function experiments were conducted to explore the modulatory effects of Foxd3, miR214 and Kcnk2 on PC12 cells under hypoxia/reoxygenation (H/R) conditions. MiR-214 and Kcnk2 were poorly expressed, while Foxd3 was highly expressed in the rat spinal cord tissues and H/R-treated PC12 cells. Kcnk2 overexpression enhanced the viability and inhibited the apoptosis of the H/R-treated PC12 cells. Notably, Foxd3 activated miR-214, and miR-214 targeted Kcnk2. In addition, upregulation of Kcnk2 or knockdown of Foxd3 promoted the cell viability and reduced the apoptosis of the H/R-treated PC12 cells. Overall, our study identified a novel mechanism of Foxd3/miR-214/Kcnk2 involving SCII, suggesting that either Foxd3 or miR-214 may be a novel target for the treatment of SCII.

목차

등록된 정보가 없습니다.

참고문헌 (0)

참고문헌 신청

함께 읽어보면 좋을 논문

논문 유사도에 따라 DBpia 가 추천하는 논문입니다. 함께 보면 좋을 연관 논문을 확인해보세요!

이 논문의 저자 정보

최근 본 자료

전체보기

댓글(0)

0