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논문 기본 정보

자료유형
학술저널
저자정보
Hyun Sook Koh (Gachon University) Jae Young Kim (Gachon University)
저널정보
대한의생명과학회 대한의생명과학회지 대한의생명과학회지 제20권 제1호
발행연도
2014.3
수록면
14 - 24 (11page)

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Hypoxia is one of the main reasons for islet apoptosis after transplantation as well as during isolation. In this study, we attempted to determine the potential usefulness of NF-κB inhibitor for suppression of hypoxia-induced β-cell apoptosis as well as the relationship between IP-10 induction and β-cell apoptosis in hypoxia. To accomplish this, we cultured the mouse pancreatic β-cell line MIN6 in hypoxia (1% O₂). Among several examined chemokines, only IP-10 mRNA expression was induced under hypoxia, and this induced IP-10 expression was due to NF-κB activity. Since a previous study suggested that IP-10 mediates β-cell apoptosis, we measured hypoxia-induced IP-10 protein and examined the effect of anti-IP-10 neutralizing Ab on hypoxia-induced β-cell apoptosis. However, IP-10 protein was not detected, and anti-IP-10 neutralizing Ab did not rescue hypoxia-induced MIN6 apoptosis, indicating that there is no relationship between hypoxia-induced IP-10 mRNA expression and hypoxia-induced β-cell apoptosis. Since it was still not clear if NF-κB functions as an apoptotic or anti-apoptotic mediator in hypoxia-induced β-cell apoptosis, we examined possible involvement of NF-κB in hypoxia-induced β-cell apoptosis. Treatment with 1 μM NF-κB inhibitor suppressed hypoxiainduced apoptosis by more than 50%, while 10 μM AP-1 or 4 μM NF-AT inhibitor did not, indicating involvement of NF-κB in hypoxia-induced β-cell apoptosis. Overall, these results suggest that IP-10 is not involved in hypoxia-induced β-cell apoptosis, and that NF-κB inhibitor can be useful for ameliorating hypoxia-induced β-cell apoptosis.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2015-500-001321419