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Post-transcriptional gene regulation by HuR and microRNAs in angiogenesis

Chang, Sung-Hee; Hla, Timothy

Current Opinion in Hematology: May 2014 - Volume 21 - Issue 3 - p 235–240
doi: 10.1097/MOH.0000000000000040
VASCULAR BIOLOGY: Edited by Thomas F. Deuel

Purpose of review This review summarizes recent findings in the area of post-transcriptional regulation of gene expression during angiogenesis, also known as new blood vessel formation. Specifically, we focus on gene regulation by HuR, an RNA-binding protein (RBP), and microRNAs (miRNAs) and their interplay, which ultimately influences cellular phenotypes of cells involved in angiogenesis.

Recent findings Recently, RBPs and miRNAs have emerged as key regulators of angiogenesis. We and others have demonstrated that the RBP HuR (a.k.a. Elavl1) stabilizes vascular endothelial growth factor-A mRNA, a potent angiogenic factor in the settings of tumor development and inflammation. However, several miRNAs were shown to modulate gene expression during developmental (miR-126), physiological (miR-126, miR-92a), and pathological angiogenesis (miR-200b, miR-132). Moreover, the interplay of HuR and miRNAs in the regulation of genes involved in angiogenesis was described. In addition, recent work suggests a new role of circulating miRNAs as paracrine mediators in angiogenesis.

Summary The elucidation of novel posttranscriptional gene regulatory mechanisms has expanded our understanding of angiogenesis in physiological and pathological conditions. We anticipate that this knowledge will ultimately lead to new insights for discovering novel therapeutic strategies to control pathological angiogenesis.

Department of Pathology and Laboratory Medicine, Center for Vascular Biology, Weill Cornell Medical College, Cornell University, New York, New York, USA

Correspondence to Timothy Hla, Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Room A607E, Weill Cornell Medical College, Cornell University, 1300 York Avenue, New York, New York 10021, USA. Tel: +1 212 746 9953; e-mail:

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