별지2) IMPACT 2015 초록접수양식

- 발표제목: 각 단어의 첫글자를 대문자로 하십시오.

- 발표자 & 저자성명: 공동저자를 쉼표로 구분해주시고 발표자는 밑줄로 표시해주십시오.

- 소속: 성명과 소속이 하나 이상일 경우 윗첨자 숫자로 구분하여 주십시오.

- 본문: 폰트 10으로 영문 2000자, 최대 1페이지가 넘지 않도록 해주십시오.

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Generation of 110kDa Cleavage Fragment of N-Cadherin Mediated by Calpain

You-Na Jang1,2,3, Yi-Sook Jung1, Soo Hwan Lee1,3, Chang-Hyun Moon1,3and Eun Joo Baik1,2,3*

1Department of Physiology, 2Chronic Inflammatory Disease Research Center, 3Brain Korea 21 for Medical Science, Ajou University School of Medicine, Suwon, 443-749, Korea

Neural-cadherin(N-cadherin) is a member of the classical cadherin family, transmembrane glycoproteins that mediated cellular recognition via a calcium-dependent homophilic binding mechanism. The intracellular domain of the cadherin interacts with □-catenin, which the stability is critical for the formation of extracellular cell-cell adhesion and the cell survival. We observed that transient focal cerebral ischemia induced the cleavage of N-cadherin, resulting in generation of about 110kDa fragment. This 110kDa fragment of N-cadherin also was generated by NMDA in cultured cortical neurons. The ionomycin, a Ca2+ionophore increased the amount of cleavage fragment of N-cadher in in dose-dependent manner. Searching for proteases responsible for the regulation of cleavage of N-cadherin, we identified calpain, acalcium-dependent protease, which is activated via NMDA receptor activation. Then pre-treatment with calpain inhibitors before exposure to NMDA or ionomycin decreased the amount of cleavage fragments. It was suggested calpain cleaved the cytosolic domain of N-cadherin. And the cleavage of N-cadherin was associated with □-catenin stability. Taken  together, our data showed cleavage of N-cadherin was involved in pathological conditions following ischemia and NMDA injury. The cleavage of N-cadherin could be modulated by calcium-activated protease, calpain. Calpain-mediated proteolysis of N-cadherin influenced □-catenin instability which might play potential roles in neuronal death.