Abstract
HuR (ELAV11 (embryonic lethal, abnormal vision)-like 1), a ubiquitously expressed member of the ELAV-like RNA-binding protein family, has been shown to regulate the stability and translation of mRNAs that encode factors regulating cellular senescence, thereby impacting on aging. In this review, we discuss the current knowledge of HuR's role in vascular cell senescence and vascular aging.
Highlights
Vascular cell senescence is defined as a state of indefinite growth cessation that accompanies the replicative exhaustion of cells or growth arrest triggered by cellular damage or oncogenic signaling [1]
It is well established that HuR binds to mRNAs bearing U-rich or AU-rich sequences (AREs), which are typically present in their 3′-untranslated regions (3′-UTRs) [5]
This review focuses on the RNA-binding protein HuR, which is involved in the regulation of turnover or translation of mRNAs encoding vascular aging-related proteins
Summary
In addition to transcriptional mechanisms, studies over the past decade have revealed that post-transcriptional gene regulation, especially through changes in mRNA turnover and translation, critically influences protein expression patterns in the senescent cell [1]. Studies over the past decade have revealed that post-transcriptional regulation, especially through control of mRNA turnover and translation, critically influences protein expression patterns in the senescent cell [1,9]. The impact of HuR upon the above regulatory factors of the cell division cycle has not been reported with respect to vascular aging; this regulation may be important for this process because reduced levels of HuR during vascular aging are accompanied by decreased levels of cyclin A and cyclin B1 as well as increased levels of p16 and p27 [6,7,18]. Because HuR, SIRT1 and VEGF levels decline with vascular aging [6,8,24], it is possible that the reduced SIRT1 and VEGF levels in senescent cells may result from the loss of
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