Involvement of ELAV RNA-binding proteins in the post-transcriptional regulation of HO-1

被引：12

作者：

Amadio, Marialaura ^{[1
]}

Scapagnini, Giovanni ^{[2
]}

Davinelli, Sergio ^{[2
]}

Calabrese, Vittorio ^{[3
,4
]}

Govoni, Stefano ^{[1
]}

Pascale, Alessia ^{[1
]}

机构：

[1] Univ Pavia, Dept Drug Sci, Pharmacol Sect, I-27100 Pavia, Italy

[2] Univ Molise, Dept Med & Hlth Sci, I-86100 Campobasso, Italy

[3] Inter Univ Consortium SannioTech, Benevento, Italy

[4] Univ Catania, Dept Biomed Sci, Catania, Italy

来源：

Frontiers in Cellular Neuroscience | 2015年 / 8卷

关键词：

hemeoxygenase-1; ELAV; hemin; post-transcriptional regulation; OXIDATIVE STRESS; HEME OXYGENASE-1; NITRIC-OXIDE; NEURODEGENERATIVE DISORDERS; GENE-EXPRESSION; BRAIN; CELLS; NEURONS; MECHANISMS; HUR;

D O I：

10.3389/fncel.2014.00459

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Heme oxygenase-1 (HO-1) is an inducible rate-controlling enzyme of heme catabolism. The cytoprotective function of HO-1 activity has been verified in multiple studies, and together with its by-products is considered a key component of the cellular stress response. The transcriptional induction of HO-1 has been largely studied in response to multiple forms of stressful stimuli but our understanding of HO-1 post-transcriptional control mechanisms in neuronal cells is currently lacking. In the present report we show the involvement of the RNA-binding proteins (RBPs) embryonic lethal abnormal vision (ELAV) in the regulation of HO-1 gene expression. Our study demonstrates a specific binding between HO-1 messenger RNA (mRNA) and ELAV proteins, accompanied by an increased expression of HO-1 at protein level, in a human neuroblastoma cell line treated with hemin. Clarifying the induction of HO-1 expression at post-transcriptional level may open therapeutic perspectives for treatments associated with the modulation of HO-1 expression.

引用

页数：5

共 32 条

[1]

Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence [J].