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CCAAT/增强子结合蛋白α足以启动3T3-L1脂肪细胞分化程序。

CCAAT/enhancer binding protein alpha is sufficient to initiate the 3T3-L1 adipocyte differentiation program.

作者信息

Lin F T, Lane M D

机构信息

Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205.

出版信息

Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8757-61. doi: 10.1073/pnas.91.19.8757.

DOI:10.1073/pnas.91.19.8757
PMID:8090719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC44685/
Abstract

Previous studies showed that CCAAT/enhancer binding protein alpha (C/EBP alpha) is required for differentiation of 3T3-L1 preadipocytes induced by exogenous hormonal agents. It was not possible to ascertain, however, whether C/EBP alpha alone is sufficient to induce differentiation because its antimitogenic activity precluded propagating 3T3-L1 cell lines that constitutively express C/EBP alpha at high levels. This problem was circumvented by using 3T3-L1 preadipocytes stably transfected with an isopropyl beta-D-thiogalactoside (IPTG)-inducible p42 C/EBP alpha expression vector system. IPTG-induced expression of the 42-kDa isoform of C/EBP alpha in preadipocytes caused expression of several endogenous adipocyte-specific genes (genes encoding the 422 adipose P2 protein, glucose transporter 4, and C/EBP alpha) and the accumulation of cytoplasmic triglyceride. Thus, C/EBP alpha is not only necessary but also is sufficient to trigger differentiation of growth-arrested 3T3-L1 preadipocytes without use of exogenous hormonal agents.

摘要

先前的研究表明，CCAAT/增强子结合蛋白α（C/EBPα）是外源性激素诱导3T3-L1前脂肪细胞分化所必需的。然而，由于其抗有丝分裂活性阻碍了组成型高水平表达C/EBPα的3T3-L1细胞系的增殖，因此无法确定单独的C/EBPα是否足以诱导分化。通过使用稳定转染异丙基β-D-硫代半乳糖苷（IPTG）诱导型p42 C/EBPα表达载体系统的3T3-L1前脂肪细胞，解决了这个问题。IPTG诱导前脂肪细胞中42 kDa C/EBPα异构体的表达，导致几种内源性脂肪细胞特异性基因（编码422脂肪P2蛋白、葡萄糖转运蛋白4和C/EBPα的基因）的表达以及细胞质甘油三酯的积累。因此，C/EBPα不仅是生长停滞的3T3-L1前脂肪细胞分化所必需的，而且在不使用外源性激素的情况下也足以触发其分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/6bc689fa32e1/pnas01141-0041-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/ce8ee658762a/pnas01141-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/9e66413acc5a/pnas01141-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/86aeedf68367/pnas01141-0040-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/e4e394b4f9de/pnas01141-0041-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/6bc689fa32e1/pnas01141-0041-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/ce8ee658762a/pnas01141-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/9e66413acc5a/pnas01141-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/86aeedf68367/pnas01141-0040-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/e4e394b4f9de/pnas01141-0041-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742a/44685/6bc689fa32e1/pnas01141-0041-b.jpg

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