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We have previously found that connexin43 is phosphorylated by extracellular-signal-regulated kinase (ERK)1/2 in rats of cerebral ischemia. Here, we investigated the potential roles of microRNA (miR)-302 cluster in the regulation of ERK1/2 mediated connexin43 phosphorylation and protection from traumatic brain injury (TBI) induced brain damage. We examined apoptosis and ERK1/2 and connexin43 phosphorylation in SH-SY5Y cells undergoing pulsatile shear stress treatment. We assessed expression of miR-302 cluster members and exogenously expressed miR-302 cluster in stressed cells to determine its effect on ERK1/2 and connexin43 phosphorylation. Finally, we investigated the effects of elevated miR-302 expression on cognitive function and brain damage in TBI rats generated by the controlled cortical impact method. Pulsatile shear stress leads to increased apoptosis and upregulation of ERK1/2 and connexin43 phosphorylation in vitro. Additionally, pulsatile shear stress significantly suppressed miR-302 expression and exogenously expression of miR-302 cluster inhibited ERK1/2 and connexin43 phosphorylation. Finally, elevated expression of miR-302 cluster not only improved cognitive function of TBI rats but also attenuated brain damage by suppressing edema and reducing contusion volume. Our study suggests that miR-302 protects rats from TBI induced brain damage and cognitive impairment and may represent an effective therapeutic strategy for TBI.
This article was published in the following journal.
Name: Journal of chemical neuroanatomy
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A form of acquired brain injury which occurs when a sudden trauma causes damage to the brain.
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Traumatic injuries to the cranium where the integrity of the skull is not compromised and no bone fragments or other objects penetrate the skull and dura mater. This frequently results in mechanical injury being transmitted to intracranial structures which may produce traumatic brain injuries, hemorrhage, or cranial nerve injury. (From Rowland, Merritt's Textbook of Neurology, 9th ed, p417)
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