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本文引用的文献

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Interleukin-15 affects differentiation and apoptosis in adipocytes: implications in obesity.白细胞介素-15影响脂肪细胞的分化和凋亡：对肥胖的影响
Lipids. 2011 Nov;46(11):1033-42. doi: 10.1007/s11745-011-3594-5. Epub 2011 Sep 6.
2
High glucose-induced repression of RAR/RXR in cardiomyocytes is mediated through oxidative stress/JNK signaling.高糖诱导的心肌细胞中 RAR/RXR 的抑制是通过氧化应激/JNK 信号通路介导的。
J Cell Physiol. 2012 Jun;227(6):2632-44. doi: 10.1002/jcp.23005.
3
Signaling by vitamin A and retinol-binding protein regulates gene expression to inhibit insulin responses.维生素 A 和视黄醇结合蛋白的信号转导调节基因表达以抑制胰岛素反应。
Proc Natl Acad Sci U S A. 2011 Mar 15;108(11):4340-5. doi: 10.1073/pnas.1011115108. Epub 2011 Feb 23.
4
Cellular retinol-binding protein type I (CRBP-I) regulates adipogenesis.细胞视黄醇结合蛋白 I（CRBP-I）调节脂肪生成。
Mol Cell Biol. 2010 Jul;30(14):3412-20. doi: 10.1128/MCB.00014-10. Epub 2010 May 24.
5
Alterations of retinol-binding protein 4 species in patients with different stages of chronic kidney disease and their relation to lipid parameters.不同慢性肾脏病分期患者视黄醇结合蛋白 4 异构体的改变及其与脂质参数的关系。
Biochem Biophys Res Commun. 2010 Feb 26;393(1):79-83. doi: 10.1016/j.bbrc.2010.01.082. Epub 2010 Jan 25.
6
Circulating retinol-binding protein 4, cardiovascular risk factors and prevalent cardiovascular disease in elderly.老年人群中循环视黄醇结合蛋白4、心血管危险因素与心血管疾病患病率
Atherosclerosis. 2009 Sep;206(1):239-44. doi: 10.1016/j.atherosclerosis.2009.02.029. Epub 2009 Mar 11.
7
Soluble adenylyl cyclase controls mitochondria-dependent apoptosis in coronary endothelial cells.可溶性腺苷酸环化酶调控冠状动脉内皮细胞中依赖线粒体的细胞凋亡。
J Biol Chem. 2009 May 29;284(22):14760-8. doi: 10.1074/jbc.M900925200. Epub 2009 Mar 31.
8
Retinol-binding protein 4 is associated with impaired glucose tolerance but not with whole body or hepatic insulin resistance in Mexican Americans.视黄醇结合蛋白4与葡萄糖耐量受损有关，但与墨西哥裔美国人的全身或肝脏胰岛素抵抗无关。
Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E758-64. doi: 10.1152/ajpendo.90737.2008. Epub 2009 Feb 3.
9
Elevated serum retinol-binding protein 4 concentrations are associated with renal dysfunction and uric acid in type 2 diabetic patients.2型糖尿病患者血清视黄醇结合蛋白4浓度升高与肾功能不全及尿酸有关。
Diabetes Metab Res Rev. 2008 Nov-Dec;24(8):629-34. doi: 10.1002/dmrr.894.
10
Evidence that kidney function but not type 2 diabetes determines retinol-binding protein 4 serum levels.肾功能而非2型糖尿病决定视黄醇结合蛋白4血清水平的证据。
Diabetes. 2008 Dec;57(12):3323-6. doi: 10.2337/db08-0866. Epub 2008 Sep 16.

游离视黄醇结合蛋白 4 浓度增加通过受体介导的信号诱导细胞凋亡。

Increased unbound retinol-binding protein 4 concentration induces apoptosis through receptor-mediated signaling.

机构信息

Graduate Institute of Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

School of Medicine, College of Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

出版信息

J Biol Chem. 2012 Mar 23;287(13):9694-9707. doi: 10.1074/jbc.M111.301721. Epub 2012 Feb 3.

DOI:10.1074/jbc.M111.301721
PMID:22308028
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3322976/
Abstract

The increase of apo-/holo-retinol-binding protein 4 (RBP4) concentrations has been found in subjects with renal dysfunction and even in diabetic patients with microalbuminuria. Holo-RBP4 is recognized to possess cytoprotective function. Therefore, we supposed that the relative increase in apo-RBP4 might induce cell damage. In this study, we investigated the signal transduction that activated apoptosis in response to the increase of apo-/holo-RBP4 concentration. We found that increase of apo-/holo-RBP4 concentration ratio delayed the displacement of RBP4 with "stimulated by retinoic acid 6" (STRA6), enhanced Janus kinase 2 (JAK2)/STAT5 cascade, up-regulated adenylate cyclase 6 (AC6), increased cAMP, enhanced JNK1/p38 cascade, suppressed CRBP-I/RARα (cellular retinol-binding protein/retinoic acid receptor α) expression, and led to apoptosis in HK-2 and human umbilical vein endothelial cells. Furthermore, STRA6, JAK2, STAT5, JNK1, or p38 siRNA and cAMP-PKA inhibitor reversed the repression of CRBP-I/RARα and apoptosis in apo-RBP4 stimulation. In conclusion, this study indicates that the increase of apo-/holo-RBP4 concentration may influence STRA6 signaling, finally causing apoptosis.

摘要

载脂蛋白/全结合视黄醇结合蛋白 4（RBP4）浓度的增加已在肾功能障碍患者中发现，甚至在伴有微量白蛋白尿的糖尿病患者中也发现了这种情况。全结合 RBP4 被认为具有细胞保护功能。因此，我们推测 apo-RBP4 的相对增加可能会诱导细胞损伤。在这项研究中，我们研究了激活细胞凋亡的信号转导，以响应 apo-/全结合 RBP4 浓度的增加。我们发现 apo-/全结合 RBP4 浓度比值的增加延迟了 RBP4 与“视黄酸 6 刺激”（STRA6）的置换，增强了 Janus 激酶 2（JAK2）/STAT5 级联反应，上调了腺苷酸环化酶 6（AC6），增加了 cAMP，增强了 JNK1/p38 级联反应，抑制了细胞视黄醇结合蛋白/维甲酸受体α（CRBP-I/RARα）的表达，并导致 HK-2 和人脐静脉内皮细胞凋亡。此外，STRA6、JAK2、STAT5、JNK1 或 p38 siRNA 和 cAMP-PKA 抑制剂逆转了 apo-RBP4 刺激对 CRBP-I/RARα 的抑制和凋亡。总之，本研究表明 apo-/全结合 RBP4 浓度的增加可能会影响 STRA6 信号转导，最终导致细胞凋亡。