Leptin activates Stat3, Stat1 and AP-1 in mouse adipose tissue
Leptin activates Stat3, Stat1 and AP-1 in mouse adipose tissue
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DOI：
10.1016/s0303-7207(00)00313-0
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发表时间：
2000-10-25
影响因子：
4.1
通讯作者：
Piccoletti, R
中科院分区：
文献类型：
--
作者：
Bendinelli, P;Maroni, P;Piccoletti, R
给野生型和ob/ob小鼠腹腔注射瘦素可迅速激活附睾部脂肪组织中的STAT1和STAT3，前者的激活程度较小。免疫印迹实验表明，瘦素处理后，细胞总抽提物中STAT3的酪氨酸磷酸化增加，并且磷酸化的蛋白移位到细胞核中。STAT1的酪氨酸磷酸化和核转位仅在ob/ob小鼠中明显。凝胶位移和超位移分析表明，瘦素激活了脂肪核提取物的SIE结合活性，其中STAT3同源二聚体是主要的络合物。STAT1/3异源二聚体和STAT1同源二聚体在野生型和ob/ob小鼠的反应中发挥了很好的作用，尽管程度较小。体内瘦素处理也诱导了脂肪组织中AP-1的结合活性，其时间进程表明，这是一种转录后诱导机制。这种影响在ob/ob小鼠中比在野生型小鼠中更大。我们的数据表明，瘦素通过触发调节基因表达的反应，在体内直接作用于脂肪组织。(C)2000爱思唯尔爱尔兰科学有限公司。保留所有权利。
Intraperitoneal leptin administration to wild-type and ob/ob mice caused a prompt activation of Stat1 and Stat3, the former to a lesser extent, in epididymal adipose tissue. Immunoblot experiments showed that tyrosine phosphorylation of Stat3 increased in total cellular extracts and that the phosphorylated protein translocated into the nucleus upon leptin treatment. Tyrosine phosphorylation and nuclear translocation of Stat1 were evident only in ob/ob mice. Gel shift and supershift analyses showed that leptin activated sis-inducible element (SIE) binding activity of adipose nuclear extracts, with Stat3 homodimer as the predominant complex. Stat1/3 heterodimers and Stat1 homodimers take part its well in the response in wild-type and ob/ob mice, although to a lesser degree. AP-1 binding activity was also induced in adipose tissue by in vivo leptin treatment with a time course that suggests a post-transcriptional inductive mechanism. This effect was greater in the ob/ob than in wild-type mice. Our data indicate that leptin operates in vivo directly on adipose tissue by triggering responses that modulate gene expression. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.