胰高血糖素样肽-2：不同的信号通路。
Glucagon-like peptide-2: divergent signaling pathways.
作者信息
Rocha Flavio G, Shen K Robert, Jasleen Jasleen, Tavakkolizadeh Ali, Zinner Michael J, Whang Edward E, Ashley Stanley W
机构信息
Department of Surgery, Brigham & Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA, USA.
出版信息
J Surg Res. 2004 Sep;121(1):5-12. doi: 10.1016/j.jss.2004.04.009.
BACKGROUND AND AIMS
Glucagon-like peptide 2 (GLP-2) is an endogenous hormone with potent and specific intestinotrophic activity in vivo and in vitro. The aim of this study was to define the initial signal transduction mechanisms mediating the proliferative actions of GLP-2 on intestinal epithelial cells.
METHODS
The proliferative actions of GLP-2 on the human Caco-2 cell line were assessed. Specific G-protein inhibitors, pertussis and cholera toxin, were used to characterize the roles of early signal transduction mechanisms in mediating the proliferative actions of GLP-2 in these cells.
RESULTS
GLP-2 directly stimulated proliferation in the Caco-2 cells. GLP-2 stimulated proliferation was (1) inhibited in a dose-dependent fashion by both pertussis and cholera toxin and (2) augmented by 2',5'-dideoxyadenosine. Proliferation rates were inversely proportional to changes in intracellular cAMP concentration.
CONCLUSIONS
Our findings suggest that a G-protein-linked signaling pathway is involved with GLP-2 bioactivity in the intestinal epithelial cell line Caco-2.
背景与目的
胰高血糖素样肽2（GLP - 2）是一种内源性激素，在体内和体外均具有强大且特异的肠营养活性。本研究旨在确定介导GLP - 2对肠上皮细胞增殖作用的初始信号转导机制。
方法
评估了GLP - 2对人Caco - 2细胞系的增殖作用。使用特异性G蛋白抑制剂百日咳毒素和霍乱毒素来表征早期信号转导机制在介导GLP - 2对这些细胞增殖作用中的作用。
结果
GLP - 2直接刺激Caco - 2细胞增殖。GLP - 2刺激的增殖（1）被百日咳毒素和霍乱毒素以剂量依赖性方式抑制，（2）被$2'$，$5'$ - 二脱氧腺苷增强。增殖率与细胞内cAMP浓度的变化呈反比。
结论
我们的研究结果表明，在肠上皮细胞系Caco - 2中，一种G蛋白偶联信号通路与GLP - 2的生物活性有关。
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