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Overexpression of translationally controlled tumor protein as a potential mechanism for lead-induced hypertension

Title
Overexpression of translationally controlled tumor protein as a potential mechanism for lead-induced hypertension
Authors
Zhou Jialan
Issue Date
2009
Department/Major
대학원 생명·약학부약학전공
Publisher
이화여자대학교 대학원
Degree
Master
Advisors
이경림
Abstract
Lead exposure is a well-known cause of hypertension in humans and experimental animals. Although different considerations have been raised to explain the pathogenesis of lead-induced hypertension, several studies have suggested that the primary involvement of the increased production of reactive oxygen species (ROS) was observed in lead-exposed animals. Increased level of ROS can be generated by the upregulation of COX-2 and catalase. To identify whether TCTP is involved in the mechanism of lead-induced hypertension, I treated lead on rat aortic smooth muscle cells, A7r5. The expression of TCTP, COX-2, and catalase was increased by the lead treatment, and its expression level was decreased by TCTP siRNA transfection. In summary, lead caused the overexpression of TCTP, COX-2 and catalase which might be involved in the generation of ROS in A7r5 cells, suggesting that TCTP is most likely involved in the pathogenesis of lead-induced hypertension.;사람을 비롯한 동물 실험 모델에서 납(lead)이 고혈압 유발인자임을 밝혔다. 납으로 야기된 고혈압의 병태 생리학적 기전을 설명하는 여러 시도 중에 활성 산소 종(ROS)의 발생이 가장 유력한 고혈압 발생 원인일 수 있다고 납(lead)중독 동물모델 연구에서 보고되었다. 활성 산소 종(ROS)은 COX-2, catalase의 증가로 발생한다. TCTP가 납(lead)으로 야기된 고혈압 발생 기작에 관여하는 지를 증명하기 위해, 나는 A7r5 세포에 납을 처리하였고 TCTP가 과발현 됨을 확인하였다. 납에 의해 TCTP가 과발현 되었을 때 COX-2, catalase의 발현도 증가하였고, TCTP를 siRNA로 knockdown 시켰을 때 COX-2, catalase의 발현도 감소되는 것을 확인하였다. 요약하여, 납이 A7r5 세포에서 활성 산소 종(ROS)을 발생 시킬 수 있는 TCTP, COX-2, calatase를 과발현 시켰으므로, 이는 TCTP가 납(lead)으로 야기된 고혈압의 병태생리학적 기전에 관여될 수 있음을 시사한다.
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