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缺氧和氯化钴对人结肠癌细胞肾上腺髓质素的诱导作用。

Induction of adrenomedullin by hypoxia and cobalt chloride in human colorectal carcinoma cells.

作者信息

Nakayama M, Takahashi K, Murakami O, Shirato K, Shibahara S

机构信息

Department of Molecular Biology and Applied Physiology, Tohoku University School of Medicine, Miyagi, Japan.

出版信息

Biochem Biophys Res Commun. 1998 Feb 13;243(2):514-7. doi: 10.1006/bbrc.1998.8131.

DOI:10.1006/bbrc.1998.8131
PMID:9480840
Abstract

Adrenomedullin (ADM) is a vasodilator peptide, first isolated from human pheochromocytoma. To explore the pathophysiological role of ADM in ischemic conditions, we investigated the effects of hypoxia on ADM production and ADM mRNA expression in a cultured human colorectal carcinoma cell line, DLD-1. Northern blot analysis and radioimmunoassay showed that hypoxia stimulated the accumulation of ADM mRNA in the DLD-1 cells and immunoreactive ADM (ir-ADM) in the cultured media. Exposure to hypoxia for 12 hours increased ADM mRNA levels about 6-fold and ir-ADM levels about 4-fold. Moreover, treatment of DLD-1 cells with cobalt chloride, which mimics hypoxic states, significantly increased ADM mRNA levels about 18-fold and ir-ADM levels about 4-fold. These results suggest that ADM plays an important role in the pathophysiology of ischemic states.

摘要

肾上腺髓质素(ADM)是一种血管舒张肽,最初从人嗜铬细胞瘤中分离出来。为了探究ADM在缺血状态下的病理生理作用,我们研究了缺氧对人结肠癌细胞系DLD-1中ADM产生及ADM mRNA表达的影响。Northern印迹分析和放射免疫测定表明,缺氧刺激了DLD-1细胞中ADM mRNA的积累以及培养基中免疫反应性ADM(ir-ADM)的产生。缺氧暴露12小时使ADM mRNA水平增加约6倍,ir-ADM水平增加约4倍。此外,用模拟缺氧状态的氯化钴处理DLD-1细胞,显著使ADM mRNA水平增加约18倍,ir-ADM水平增加约4倍。这些结果表明,ADM在缺血状态的病理生理过程中起重要作用。

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