We need followup research which is so easy to accomplish. You put an RFP out to researchers, pay for it with foundation grants and write the results up in a stroke protocol available in a public database.
- SIGNIFICANCE
In this review, the role of miR-17–92 cluster in neuronal and vascular
plasticity, and its potential as a novel therapeutic target for CNS
injury are discussed.
- This
work was supported by grants from the National Natural Science
Foundation of China (NSFC, 81171719) and from Chongqing Natural Science
of Foundation of China (CSTC, 2008 BB5281).
Abstract
It
is well known that neurogenesis is not the only concern for the fully
functional recovery after brain or spinal cord injury, as it has been
shed light on the critical role of angiogenesis in improving
neurological functional recovery. Angiogenesis and neurogenesis
coordinately interact with each other in the developing and adult brain,
during which they may respond to similar mediators and receptors, in
which they share a common posttranscriptional regulator: the miR-17–92
cluster. The miR-17–92 cluster was initially described as an oncogene
and was later demonstrated to drive key physiological and pathological
responses during development and diseases respectively. It has been
reported that the miR-17–92 cluster regulates both neurogenesis and
angiogenesis. The miR-17–92 cluster modulates neural progenitor cells
proliferation not only during development but also during neurological
disorders such as stroke. It has also been shown that the endothelial
miR-17–92 cluster regulates angiogenesis during embryonic stage and
adulthood. In this review, we have discussed the actions of the
miR-17–92 cluster in neuronal and vascular plasticity, and its potential
as a novel therapeutic strategy for CNS injury. © 2016 Wiley
Periodicals, Inc.
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