小鼠乳腺中瘦素的信号转导通路

Study on signal transduction pathway of leptin in mammary gland of mouse

为研究小鼠乳腺发育、泌乳和退化过程中瘦素的信号转导通路,分别取妊娠12d、泌乳12d以及退化12d小鼠乳腺组织进行体外培养,对照组培养基为无血清培养基,处理组培养基中则只添加瘦素。培养48 h后取出分别提取乳腺上皮细胞总蛋白,并用免疫印迹的方法检测对照组和处理组乳腺上皮细胞中信号分子MAPK、STAT3和STAT5的磷酸化情况。结果表明,虽然在妊娠期、泌乳期和退化期乳腺上皮细胞中均有MAPK、STAT3和STAT5信号分子存在,但是在妊娠期瘦素只能专一性的诱导MAPK磷酸化,泌乳期瘦素可以激活STAT3和STAT5,而在退化期瘦素则特异性地激活STAT3,启动乳腺上皮细胞的凋亡过程。

To determine the signal transduction pathway of leptin in mammary gland. The mammary gland of mouse about 12 days of pregnancy, lactation and involution were cultured in vitro. Each individual gland was placed in a 3.5 cm culture well and cultured for 48 h in the media Waymouth＇s MB752/1 with or without leptin. Following 48 h in culture, each gland was digested to obtain epithelial cells. Then the cells were lysed and the lysate was used for western blot analysis. Western blot results showed that although MAPK, STAT3 and STATS existed in the epithelial cells of mammary gland, leptin only activated MAPK in pregnancy and activated STAT3 and STAT5 in lactation. In involution, leptin induced STAT3 phosphorylation specificly to initiate postlactational apoptosis.