Heart-type fatty-acid-binding protein (FABP3) is a lysophosphatidic acid-binding protein in human coronary artery endothelial cells.
Heart-type fatty-acid-binding protein (FABP3) is a lysophosphatidic acid-binding protein in human coronary artery endothelial cells.
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DOI：
10.1016/j.fob.2014.10.014
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发表时间：
2014
期刊：
影响因子：
2.6
通讯作者：
Tsukahara, Tamotsu
中科院分区：
文献类型：
--
作者：
Tsukahara, Ryoko;Haniu, Hisao;Matsuda, Yoshikazu;Tsukahara, Tamotsu
我们已经确定FABP 3作为LPA载体蛋白在人冠状动脉内皮细胞（HCAECs）。LPA对HCAEC的给药导致PPARγ活化的剂量依赖性增加。当使用小干扰RNA（siRNA）降低FABP 3表达时，LPA诱导的PPARγ活化被消除。FABP 3通过将LPA靶向至细胞核中的同源过氧化物酶体增殖物激活受体γ来控制LPA的转录活性。脂肪酸结合蛋白3，肌肉和心脏（Fatty-acid-binding protein 3，muscle and heart，FABP 3），也称为心脏型FABP，是细胞内脂质结合蛋白家族的成员。它是一种小的细胞质蛋白，分子量约为15 kDa。已知FABP是用于将脂肪酸和其它亲脂性物质从细胞质转运至细胞核的载体蛋白，在细胞核中这些脂质被释放至一组核受体，例如过氧化物酶体增殖物激活受体（PPARs）。在这项研究中，使用溶血磷脂酸（LPA）包被的琼脂糖珠，我们已经确定FABP 3作为LPA载体蛋白在人冠状动脉内皮细胞（HCAECs）。LPA对HCAEC的给药导致PPARγ活化的剂量依赖性增加。此外，当使用小干扰RNA（siRNA）降低FABP 3表达时，LPA诱导的PPARγ活化被消除。我们进一步表明，对照HCAECs的核部分含有大量的外源性添加的LPA，而FABP 3 siRNA转染的HCAECs在核中的LPA水平降低。综上所述，这些结果表明FABP 3通过靶向细胞核中的同源PPARγ来控制LPA的转录活性。
We have identified FABP3 as an LPA carrier protein in human coronary artery endothelial cells (HCAECs). Administration of LPA to HCAECs resulted in a dose-dependent increase in PPARγ activation. LPA-induced PPARγ activation was abolished when the FABP3 expression was reduced using small interfering RNA (siRNA). FABP3 governs the transcriptional activities of LPA by targeting them to cognate PPARγ in the nucleus. Fatty-acid-binding protein 3, muscle and heart (FABP3), also known as heart-type FABP, is a member of the family of intracellular lipid-binding proteins. It is a small cytoplasmic protein with a molecular mass of about 15 kDa. FABPs are known to be carrier proteins for transporting fatty acids and other lipophilic substances from the cytoplasm to the nucleus, where these lipids are released to a group of nuclear receptors such as peroxisome proliferator-activated receptors (PPARs). In this study, using lysophosphatidic acid (LPA)-coated agarose beads, we have identified FABP3 as an LPA carrier protein in human coronary artery endothelial cells (HCAECs). Administration of LPA to HCAECs resulted in a dose-dependent increase in PPARγ activation. Furthermore, the LPA-induced PPARγ activation was abolished when the FABP3 expression was reduced using small interfering RNA (siRNA). We further show that the nuclear fraction of control HCAECs contained a significant amount of exogenously added LPA, whereas FABP3 siRNA-transfected HCAECs had a decreased level of LPA in the nucleus. Taken together, these results suggest that FABP3 governs the transcriptional activities of LPA by targeting them to cognate PPARγ in the nucleus.
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影响因子：
4.8
作者：
Binas, B;Danneberg, H;Clark, AJ
通讯作者：
Clark, AJ
影响因子：
7.7
作者：
Spiegelman, BM
通讯作者：
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影响因子：
64.8
作者：
Kersten, S;Desvergne, B;Wahli, W
通讯作者：
Wahli, W
DOI：
10.1073/pnas.0135855100
发表时间：
2003-01-07
影响因子：
11.1
作者：
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通讯作者：
Prestwich, GD
影响因子：
7.7
作者：
Shearer, J;Fueger, PT;Rottman, JN
通讯作者：
Rottman, JN